Our finding that somatic expression of PIK3CAH1047R—by a lentivector or via genome editing—led to swift tumor formation in MMTV-Wnt1 mice (Fig. 4) suggests that PIK3CA activation collaborates with Wnt1 signaling in mammary tumorigenesis and, as a well-recognized downstream mediator of RAS signaling, can even substitute for RAS in transforming WNT1-activated mammary tumors. This evidence concerns the gene PIK3CA and neoplasm.