It should be noted that the binding of c-Abl to the C terminus of wild-type p53 is well established, and necessary for proper transactivation and growth suppression by p53.33, 34 Similarly, deletion of the p53-binding domain of c-Abl prevents the transactivation of p53 and its ability to inhibit proliferative programs.33 Collectively, it stands to reason that dysregulation of either c-Abl or p53 disrupts their respective tumor suppressive functions, leading to the development and progression of TNBCs (e.g., MDA-MB-231 cells). Here, ABL1 is linked to neoplasm.