G0S2 and exocrine pancreatic carcinoma: Mechanistically, the mutation of UTX partially lost its histone H3K27 demethylase and elevated the H3K27me3 modification level of the G0S2 promoter, which decreased its expression and promoted the Toll-like/MAPK signaling pathway to weaken the antitumor effect of wild-type UTX in pancreatic carcinoma.