A well-characterized class of chromatin alterations in response to DNA damage, nucleotide excision repair, was delineated uniquely at the interface of luminal A and B (ER+), through CUL4B, XPA, XPC, MMS19, and RNF111 in luminal A, and XPA, RFC1, ERCC8, XPC, RNF111, SIRT1, and POLK in luminal B. Mutations in nucleotide excision repair genes are suggested as drivers of ER+ cancers [51]. This evidence concerns the gene POLK and cancer.