Our previous findings identified c-Abl as a robust and multifaceted tumor suppressor whose anticancer activities are dependent upon the mutational and expression status of p53.10, 11 The mitotic kinase, TTK, is overexpressed in mutant p53-expressing TNBCs and has been shown to regulate the cellular localization of c-Abl in response to oxidative stress.14, 15, 16, 17, 18, 21 Herein, we also established p53 expression (wild-type or mutant) as an essential determinant for the correlation between c-Abl and TTK expression across all breast cancer subtypes. Here, ABL1 is linked to neoplasm.