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). Here, FOXA1 is linked to breast neoplasm.