In acute myeloid leukemia, VEGFR2 inhibition enhanced cell sensitivity to chemotherapy in a PGC1α-dependent manner with increased mitochondrial mass [36], while the depletion of PGC1α abolished such induction of mitochondrial metabolism and chemosensitization in response to VEGFR2 inhibition. The gene discussed is KDR; the disease is acute myeloid leukemia.