When we analyzed mitochondrial content in iNOS-deficient MDA-MB-231 breast cancer tumors (59) from a previous study (5), the loss of EPOR in these tumors did not influence mitochondrial content or transcriptional regulators of mitochondrial biogenesis, suggesting that iNOS expression is essential for EPOR-dependent control of mitochondrial biogenesis. This evidence concerns the gene EPOR and breast carcinoma.