Consistent with these observations, we found that BPTES treatment elevated AREG expression in HEK293T cells containing inactive p53 and in p53-deficient PC3 human prostate cancer cells (Fig. 3b and Supplementary Fig. 3a), suggesting that p53 is unlikely to account for the observed AREG regulation by mitochondrial Gln metabolism. The gene discussed is TP53; the disease is prostate carcinoma.