AKR1A1 and diabetes mellitus: reported that the detoxification of toxic aldehydes, for example, ACR, is a principal function for Akr1a1, and overexpression of Akr1a1 alleviates the Tg MEF’s (transgenic Mouse Embryonic Fibroblasts) sensitivity to ACR.[29] In a previous study, Akr1a1b was identified as a gluconeogenesis regulator via adjusting S‐nitrosyaltion in zebrafish.[26] However, whether Akr1a1a functions closely to Akr1a1b or completely separate and whether a permanent loss of Akr1a1a causes accumulated internal ACR and results in diabetes and relevant complications in the end require further elucidation.