In line with previous studies linking GLS-driven glutamine catabolism to the occurrence and progression of prostate cancer and pancreatic cancer [35, 36], as well as enhanced glutamine hydrolysis driving hypoxia-induced chemoresistance in pancreatic cancer [37], we hypothesize that RPS27-RPS24 may promote glutamine metabolism by upregulating GLS expression, which may be closely associated with OSchemoresistance and copper death. Here, GLS is linked to familial pancreatic carcinoma.