ANP32E and breast neoplasm: In Basal-L/TNBC tumors, largely believed to arise from a more stem-like multipotent progenitor, high levels of ANP32E ‘lock-in’ a pattern of accessible chromatin that favors proliferation and self-renewal, while in HR+ breast tumors, arising in a more differentiated luminal progenitor, ANP32E supports the maintenance of luminal identity and hormone responsiveness by restricting FOXA1 binding at estrogen response elements (Fig. 5).