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KRAS mutations in pancreatic cancer cells rely on both endogenous TNF -related apoptosis-inducing ligands (TRAILs) as well as their receptors to promote tumor growth and metastasis ( KRAS mutations evaded immune therapy by upregulating programmed cell death 1 ligand 1 (PD-L1) transcription and protein expression ( KRAS mutation could also enhance the recycling of PD-L1 molecules in pancreatic cancer cells to the cell surface to promote the immune escape of pancreatic cancer cells ( KRAS mutation-containing PDAC tumors displayed high m6A scores, suggesting a correlation between KRAS , m6A, and immune escape (Figure 7)

Yamamura S, Izumiya Y, Araki S, Nakamura T, Kimura Y, Hanatani S, et al

These results revealed an antioxidant effect through Nrf2-mediated HO-1 induction

Disruption of mitochondrial complex I induces progressive parkinsonism