Overexpression of (P)RR may contribute to cancer initiation and progression via the Wnt/β-catenin, RAS, mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK), and phosphatidylinositol 3-kinase-protein kinase/protein kinase B/mammalian target of rapamycin pathways, as well as to V-ATPase function in various cancers42. This evidence concerns the gene MTOR and cancer.