The observations that CCND1/CDK2 expression can cause TGF-β resistance in mink lung epithelial and MMTVD1-K2 mouse mammary tumor cells, and that CDK2 phosphorylation of MYC abrogates RAS-mediated OIS may explain how constitutive CCND1/CDK2 activity could replace exogenous MYC overexpression and contribute to RAS driven HMEC transformation to AIG in our protocol [22], [23], [29], [30]. This evidence concerns the gene CDK2 and breast cancer.