Recently, it was shown that blocking VEGF receptor 2 (VEGFR2) signaling sensitized chemoAML (human AML cells from terminally ill mice treated with chemotherapy) to chemotherapy by inducing a transcriptional program that promotes mitochondria biogenesis associated with increased oxidative stress, further suggesting mitochondria function is a vulnerable target for chemotherapy in AML [119]. The gene discussed is KDR; the disease is acute myeloid leukemia.