First, as pure nonsteroidal antiestrogens have been found to antagonize the proliferative activity of E2 by promoting the upregulation of p21WAF1/CIP1 and p27Kip1 expression and their nuclear recruitment into cyclin E-Cdk2 complexes,43, 44 it appears reasonable to suggest that an analogous p21WAF1/CIP1/p27Kip1-dependent cell growth-arresting mechanism might occur in response to C75-induced ablation of FASN signaling in E2-dependent breast cancer cells. The gene discussed is CDK2; the disease is breast cancer.