Although the KRAS gene is aberrantly mutated such that the KRAS protein loses its intrinsic deactivating GTPase activity and thus drives only about 5% of breast cancer cases, the downregulation of RASA1, which is the GTPase-activating protein (GAP) that promotes KRAS deactivation through GTP hydrolysis [25,26], implies that KRAS is a significant contributor to cancer progression in 77% of TNBC. This evidence concerns the gene RASA1 and breast carcinoma.