Visceral adiposity results from adipocyte hyperplasia and/or hypertrophy, and is correlated with the accumulation of pro-inflammatory macrophages that release inflammatory cytokines, triggering altered insulin signaling and sensitivity, which are key factors in determining the risk for the development of metabolic diseases, notably Type 2 diabetes mellitus (T2DM) [1]. The gene discussed is INS; the disease is type 2 diabetes mellitus.