For instance, through single-cell sequencing of mouse pancreatic tumors and experiments testing metabolic function, a study focused on the epigenetic regulation of CAFs revealed that pancreatic tumor cells with a KRAS mutation combined with SETD2 deficiency exhibit metabolism predominantly based on oxidative phosphorylation [62], in contrast to tumor cells with KRAS combined with P53 mutations, which primarily utilize glycolytic metabolism [113]. Here, KRAS is linked to pancreatic neoplasm.