For instance, loss of HNRNPM has been shown to induce splicing perturbations and contribute to lung cancer pathogenesis [26], whereas in CRC, its function is largely determined by the SUMOylation status of lysine 17 (K17), with the SUMOylated form impeding cancer cell glycolysis and tumorigenesis [45]. This evidence concerns the gene HNRNPM and lung carcinoma.