Mutual transcription factors revealed by these searches included nuclear hormone receptors (AR, ESR1), inflammatory response mediators (NFE2L2) and the DDR master regulator, TP53, demonstrating that genes critical to the cellular responses to DNA damage and stress are also susceptible to the DNA damage and aberrant repair that underpins tumourigenesis and clonal evolution in cancer (Supplementary Figure S8I). This evidence concerns the gene AR and cancer.