The HP1α-STAT1 axis was further validated to inhibit the proliferation of ICCA cells in vivo and in vitro via the induction of IFN signaling and upregulation of ISGs, which seemed to conflict with the consequence of stemness maintenance arising from the passive regulation of STAT1 and IFN signaling in breast cancer [43, 44]. This evidence concerns the gene CBX5 and breast carcinoma.