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]. The gene discussed is CCND1; the disease is breast cancer.