Stimulated ferroptosis promotes the phosphorylation of c-Jun and inhibits the modification of c-Jun by O-GlcNAc, while the overexpression of c-Jun modified by O-GlcNAc can stimulate GSH synthesis by increasing the transcription of phosphoserine aminotransferase 1 (PSAT1) and cystathionine-beta-synthase (CBS), thereby suppressing ferroptosis, deregulating the negative regulatory state of c-Jun, thereby promoting HCC development [135]. This evidence concerns the gene JUN and hepatocellular carcinoma.