Thus, individuals exposed to early life adversity may be more likely to increase their monocyte population in the context of stress, and these monocytes may be predisposed to differentiate into immune cells that behave like the non-classical CD16+ subpopulation which disproportionately secrete TNF-α [55]—the cytokine most robustly linked to early life adversity among adults [12]—become senescent [56], and contribute to disease processes such as atherosclerosis [57]. This evidence concerns the gene FCGR3A and atherosclerosis.