This abnormal accumulation of PLIN2 and PLIN5 and, by extension, of LDs in β‐cells is similar to that in hepatocytes in fatty liver disease or macrophages in atherosclerosis, where it is usually linked to the abnormal lipid catabolism.27 This prompted us to investigate whether the observed LD accumulation in T2D is accompanied and perhaps caused by an impaired processing of lipids in β‐cells. The gene discussed is PLIN5; the disease is atherosclerosis.