Exposure of prostate cancer cells to CAFS induces phosphorylation and oxidation of PKM2; after modification, the protein loses its metabolic function and acquire the ability to migrate into the nucleus, to interact with the hypoxia inducible factor 1α (HIF1α) and the protein DEC1, to inhibit transcription of a specific microRNA (mir-205) driving the metabolic conversion to OXPHOS of prostate cancer cells (Fiaschi et al., 2012; Giannoni et al., 2015). The gene discussed is HIF1A; the disease is prostate carcinoma.