We further propose that iadademstat might functionally deplete tumor-initiating CSC-like cellular states that sustain tumorigenicity by impacting on fundamental controllers of cell fate choice, an epigenetic mechanism involving both the downregulation of SOX2 and the re-activation of epigenetically suppressed differentiation programs in SOX2-enriched breast cancer subtypes such as Luminal-B and HER2-positive. The gene discussed is SOX2; the disease is neoplasm.