CBFB and breast neoplasm: Because NOTCH3 repression is a major response to CBFB loss-of-function, patients with breast tumors carrying CBFB mutations probably may benefit more from NOTCH inhibitors than those with tumors bearing wild-type CBFB. The cooperation between TAp73 loss and NOTCH3 OE raises the possibility of inhibiting breast tumorigenesis by simultaneously targeting TAp73 and NOTCH3.