Mutations in patient SA97V5 (breast cancer anti-estrogen resistance protein 1, BCAR1 mutation; ankyrin-2, ANK2 mutation; insulin receptor substrate 1, IRS1 mutation; and cAMP response element-binding binding protein, CREBBP mutation), patient 26YMUF (rapamycin-insensitive companion of TOR, RICTOR mutation and ERK mutation), and patient L6ADEL (TP53 mutation and TNF receptor-associated factor, TRAF3 mutation) all had non-KRAS and non-B-Raf proto-oncogene (BRAF) driven activation pathways of PD-1 drug responder status. This evidence concerns the gene ANK2 and breast carcinoma.