We previously demonstrated the ability of c-Abl to inhibit oncogenic TGF-β signaling in TNBCs,10 an event requiring c-Abl to activate an autocrine TGF-β1-dependent Smad2:Smad1/5/8 signaling axis that reactivated p53 expression and led to the induction of a p21-dependent senescent reaction.11 Interestingly, although c-Abl and p53 are co-expressed in normal mammary tissues, we observed both proteins to be expressed in a highly discordant manner in human breast cancers. The gene discussed is TGFB1; the disease is breast carcinoma.