The presence of cancer driven mutations like p53MUT and KRASMUT or overactivation of v-myc avian myelocytomatosis viral oncogene homolog (MYC) and mechanistic target of rapamycin kinase (mTOR) in cancer cells activates PyM-associated genes (Pugacheva et al., 2002; Liu et al., 2008; Ben-Sahra et al., 2013; Santana-Codina et al., 2018). This evidence concerns the gene MYC and cancer.