We propose that in breast cancer cells, NTX and PRO treatment causes G2/M phase cell cycle arrest by the downregulation of CDK1, the phosphorylation of CDK1 (activity) and cyclin B1 levels, the upregulation of pro-apoptotic p-Bim and effector proteins such as Bax and p-Bax, and increased levels of effector caspase 3 and CC3. The gene discussed is CASP3; the disease is breast carcinoma.