Daniel Notterman is interested in the reciprocal interactions between genetic variants and environmental signals in the developing behavioral, cognitive and emotional phenotype of the child. Over the past decade, technical advances in our ability to specify and analyze both genetic variants and epigenetic modifications to DNA and histones have enabled a new field that can be termed, social and behavioral genomics. Although this field is in its infancy, we already understand that there are robust interactions between specific genetic variants, environmental signals, and resulting behavioral and health outcomes. For example, we recently showed that women with a short, hypomorphic form of the promotor region of HTT (serotonin transporter) are more likely to experience post-partum depression in stressful socioeconomic circumstances then they are in more stable environments. However, women with the major allele of this gene (long promotor) do not display this environment-based difference in rate of postpartum depression. This is consistent with the idea that some gene variants express proteins that enhance an organism’s sensitivity to the environment—so called “reactive alleles.” These reactive alleles are the biological substrate, perhaps, for Belsky’s “Differential Sensitivity Hypothesis.” It is also known that variations in environmental input induce longstanding behavioral changes by affecting the methylation state of DNA. For example, rat pups raised by inattentive as opposed to attentive mothers have hypermethylated promoters for the GC receptor gene expressed in the hypothalamus—this reduces expression of that receptor, thereby upregulating the activity of the cortisol stress pathway in these pups. There is great excitement around findings such as this, because it points the way to a biological understanding—invoking epigenetic mechanisms—of the relationship between adverse or favorable early environments and lifelong behavioral traits.