Madan et al. (2019), studying the relation between the major TFs HIF1α and p53, showed that activated HIF1α induces p53 expression, but this HIF1α-induced p53 is transcriptionally inefficient and serves as a molecular chaperone for HIF1α, stabilizes it and, finally, promotes transcription of HIF target genes that contribute to hypoxia-induced growth and survival of cancer cells, including BC cells [138]. The gene discussed is TP53; the disease is breast cancer.