In the context of diabetes and obesity, adipocytes, endothelial cells, and infiltrated macrophages produce ANGPTL2 leading to an inflammatory response mediated through activation of the NFκB pathway: ANGPTL2 binds to integrin α5β1, activates Rac1, and thus translocates NFκB to the nucleus by increasing the degradation of its inhibitor IκB, resulting in NFκB-dependent inflammatory gene expression [5]. This evidence concerns the gene NFKB1 and diabetes mellitus.