Given that HRAS Q61 hotspot mutations are vanishingly rare in common forms of breast cancers (Fig. 3b), but present in the majority of ER-negative adenomyoepitheliomas and always in conjunction with PIK3CA or PIK3R1 somatic mutations, we posited that HRAS Q61 hotspot mutations would not only constitute an oncogenic driver of ER-negative adenomyoepitheliomas, but also play a role in the acquisition of an adenomyoepithelial phenotype. The gene discussed is PIK3CA; the disease is breast carcinoma.