Charney describes several mechanisms that will bias estimates of heritability in unpredictable directions. In addition, the mechanisms described by Charney explain the puzzling fact that research in human-behavior genetics routinely reports higher heritabilities than animal studies do. However, I argue that the concept of heritability has no real place in human research anyway.

Traditional lay perceptions of genetics are plagued with essentialist biases leading to some unfortunate consequences. Changes in the scientific understanding of heredity in general, and in genotype–phenotype relationships more specifically, provide a vital basis for shifting public understanding of genetics. Facilitating postgenomic literacy among the public has the potential to have translational implications in diminishing deleterious attitudes, beliefs, and behaviors.

The target article by Charney on behavior genetics/genomics discusses how numerous molecular factors can inform heritability estimations and genetic association studies. These factors find application in the search for genes for behavioral phenotypes, including neuropsychiatric disorders. We elaborate upon how single causal factors can generate multiple phenotypes, and discuss how multiple causal factors may converge on common neurodevelopmental mechanisms.

The plasticity of the genome complicates genetic causation but should be investigated from a functional perspective. Specific adaptive hypotheses are referenced in the target article, but it is also necessary to explain how the integrity of the genome is maintained despite processes that tend towards its diversification and degradation. These include the accumulation of deleterious changes and intragenomic conflict.

Against the opinion that DNA as program is not sufficiently explanatory, we maintain that the cellular machinery is entirely computational, and we identify the crucial notion of the interpreter that expresses the gene with the minimal gene set. Epigenetics research does not so much need paradigm shifts as the unraveling of an exceedingly complex computational machine.

Charney discusses the growing realization in the postgenomic era that genomic biology deviates from Mendelian assumptions at the heart of genetic heritability and association studies. Given the complexity of genomic biology, how are we to identify meaningful genetic factors that contribute to behavioral? One response is to make genetic variants the focus of biological rather than statistical analyses of behavior.

More than 40 years ago, Gilbert Gottlieb and like-minded scholars argued for the philosophical necessity of approaching genetic contributions to development through a multilevel, bidirectional systems perspective. Charney's target article builds on this heritage in significant ways, offering more recent examples of the interactions of biology and context, as well as the diversity of developmental mechanisms, and reaffirming a way forward for genetic research.

The target article by Charney convincingly argues that genomic plasticity perinatally induced by the environment creates a complication in determining which parts of behavior are attributed to nature and which to nurture. I argue that real life is even more complex because (1) genotype influences sensitivity to environmental stimuli, and (2) the genome continues to be modified throughout life.

Charney's target article continues a critique of genetic blueprint models of development that suggests reconsideration of concepts of adaptation, inheritance, and environment, which can be well illustrated in current research on infant attachment. The concepts of development and adaptation are so heavily based on the model of genetics and inheritance forged in the modern synthesis that they will require reconsideration to accommodate epigenetic inheritance.

Documenting the bidirectional traffic from gene action to the external environment and its effects on behavior remains a major conceptual, empirical, and analytical challenge for developmental science. Charney has provided an instructive snapshot of where we are in meeting this challenge and, in so doing, exposes the considerable shortcomings of the traditional genomic model employed by behavior genetics.

This commentary argues that age changes in heritability are incompatible with Charney's theory. The new genetics must be tempered by the findings that many epigenetic phenomena are random and are linked to pathology, thus making them peripheral to the design of complex adaptations. Behavior-genetic findings are compatible with strong maternal effects; G × E correlations likely underestimate environmental effects; and G × E interactions are unlikely to be an important aspect of normal development.

Charney's target article convincingly demonstrates the need for the discipline of quantitative human behavior genetics to discard its false assumptions and to employ the techniques, assumptions, and research program characteristic of modern developmental psychobiology.

Charney's dismissal of well-established methods in behavioral genetic research is misguided. He claims that studies of heritability and genetic association depend for their validity on six assumptions, but he cites no sources to support this claim. We explain why none of the six assumptions is strictly necessary for the utility of either method of genetic analysis.

Generalization of the standard behavior longitudinal genetic factor model for the analysis of interindividual phenotypic variation to a genetic state space model for the analysis of intraindividual variation enables the possibility to estimate subject-specific heritabilities.

Behavioural phenotypes have been explained by genetic and environmental factors (E) and their interaction. Here we suggest a rethinking of the E factor. Passively incurred environmental influences (Epass) and actively copied information and behaviour (Eact) may be distinguished at shared and non-shared level. We argue that Eact underlies mutation and selection and is the base of gene-independent heritability.

This commentary argues that the anomalies suffered by the population behavior genetics paradigm are more widespread than suggested by Charney, including many made in the field of developmental science. Further, it is argued that, according to the criteria established by Kuhn, there is and has been available an alternative scientific paradigm that provides the formative context for Charney's postgenomic view. This is the relational developmental systems paradigm.

It is worthy to supplement Charney with two historical issues: (1) There were two rival trends in the rebirth of genetic thought in the 1960s: the universal and the variation related. This traditional duality suggested that heredity cannot be equated with genetic determinism. (2) The classical debates and reinterpretation of adoption/twin studies in the 1980s regarding intelligence suggested that the environment had a more active role in unfolding the genetic program.

Several recent research findings have implicated brain-derived neurotrophic factor (BDNF) as a mediator of neuronal plasticity. The BDNF gene is under extensive epigenetic regulation, which modulates how much or how little environmental experiences become encoded within neurons and neural circuits. Future scientific progress within the postgenomic paradigm requires elucidation of the functional trajectory in neogenetic and environment interactions.

Critically significant parental effects in behavioral genetics may be partly understood as a consequence of maternal brain structure and function of caregiving systems recently studied in humans as well as rodents. Key parental brain areas regulate emotions, motivation/reward, and decision making, as well as more complex social-cognitive circuits. Additional key environmental factors must include socioeconomic status and paternal brain physiology. These have implications for developmental and evolutionary biology as well as public policy.

We address current needs for neogenomics-based theoretical and computational approaches for several neuroscience research fields, from investigations of heritability properties, passing by investigations of spatiotemporal dynamics in the neuromodulatory microcircuits involved in perceptual learning and attentional shifts, to the application of genetic algorithms to create robots exhibiting ongoing emergence.