“…More specifically, PABC epithelial cells are characterized by an increased expression of various oncogenes (e.g., MYC, SRC, FOS), tumor suppressor genes (e.g., TP53, PTEN, CAV1), apoptosis regulators (e.g., PDCD4, BLC2, BIRC5), transcription regulators (e.g., JUN, KLF1, SP110), genes associated with DNA repair mechanisms (e.g., Sig20, BRCA1/2, FEN1), cell proliferation genes (e.g., AURKA, MKI67), and genes regulating the activation of immune response (e.g., PD1, PDL1) [ 37 , 38 ]. Furthermore, PABC is associated with a significantly higher frequency of non-silent mutations and mutations in the mucin gene family [ 39 ], as well as with an increased prevalence of germline mutations in genes that are known to predispose one to cancer (especially BRCA1 and CHEK2) [ 40 ]. A summary of the potential mechanisms involved in the pathogenesis of PABC is presented at Table 2 .…”