2‐AAA treatment stimulated insulin secretion from BTC6 cells as well as isolated mouse and human islets.[19] Another study revealed that elevated levels of 2‐AAA correlated with obesity and impaired insulin signaling.[72] In this study, 2‐AAA treatment significantly promoted gluconeogenesis in primary mouse hepatocytes involved in increased expressions of Pck1 and amino acid metabolism genes through H2BK12Cr modification. The gene discussed is PCK1; the disease is obesity due to melanocortin 4 receptor deficiency.