Consistent with the inhibitor studies, stable silencing of Nrf2 supressed proliferation, glucose consumption, and the basal and maximal OCRs in Cpt1a-deficient ErbB2+ tumor cells (Fig. 5f–j, and Supplementary Fig. 8c, e), but had minimal effects on wild-type cells, arguing that Nrf2 is present but not essential in these cells. This evidence concerns the gene NFE2L2 and neoplasm.