Furthermore, low early-life SES was also shown to affect the expression of stress related genes: FKBP5 [107] OXTR [108] and AVP and inflammation associated genes: CD1D and CCL1. As such, SES would appear to act on inflammatory pathways that are common to low SES environments and eventually T2D, and may worsen the T2D etiopathology by targeting prominent pathophysiological factors like stress and inflammation. This evidence concerns the gene CD1D and type 2 diabetes mellitus.