will push these models out of accessible immune cells and into the more sensitive CNS structures that shape social, cognitive, and affective processes. It will also be critical to define the particular features of social environments that trigger transcriptional remodeling of specific cells. Given the key role of neuroendocrine responses in mediating these effects, the most decisive influences may involve our psychological reactions to social conditions rather than the properties of the external condition per se. After all, it is the subjective perception of conditions as threatening or uncertain that directly triggers SNS and HPA responses (Sapolsky, 1994). Our genome’s social sensitivity ultimately stems from the capacity of social conditions to affect CNS perceptions of safety vs. threat (Dickerson & Kemeny, 2004), and thereby trigger biological stress responses that alter gene transcription.
