According to several reports, ASCs derived from patients with morbid obesity exhibit amplified secretion levels of various pro-inflammatory cytokines like IL-6, IL-1β, IL-17 and TNF-α, diminished immunomodulatory ability, impaired proliferation, clonogenicity and suppressed expression of stemness and differentiation related genes, which denote the critical potential of obesity to elicit molecular alterations in ASCs to promote chronic low-grade systemic inflammation, and ultimately failure in adipocyte insulin response [21–23]. The gene discussed is INS; the disease is Obesity.