Moreover, resistances to chemotherapy and targeted therapies appear to be generally coupled with an increase in OXPHOS, and OXPHOS inhibition overcomes resistance to docetaxel in prostate cancer, cytarabine in acute myeloid leukemia, 5-fluorouracil in colorectal and MYC/PGC-1α-driven pancreatic cancer, to EGFR inhibition in EGFR-driven lung adenocarcinoma and MAPK or BRAF inhibition in BRAF-mutant melanoma [24, 111–114]. This evidence concerns the gene PPARGC1A and prostate carcinoma.