GOT1 and pancreatic ductal adenocarcinoma: indicated that aspartate aminotransferase (GOT1) could damage mitochondrial oxidative phosphorylation and promote catabolism, resulting in the increase of unstable iron pool and susceptibility to ferroptosis, this effect suggests that inhibiting GOT1 could destroy the redox balance and proliferation in pancreatic ductal carcinoma, and establishes a biochemical link between GOT1 and ferroptosis (132).