Moreover, our results provide a mechanistic explanation, and expand upon previous observations, of the increase in the abundance of TCA intermediates in BRCA1‐ and p53‐deficient cancer models (Breitkopf et al, 2017) and of the higher mitochondrial metabolic rate observed in MCF10A BRCA1 haplo‐insufficient cells (Cuyas et al, 2016). This evidence concerns the gene TP53 and cancer.