These differential responses likely reflect the interaction between the distinct chemical compositions of RV1 (glutamic acid/alanine/serine-rich) and RV2 (glycine/proline-rich) with the molecular backgrounds of different breast cancer subtypes, potentially involving modulation of key cell cycle regulators such as p53, cyclin D1, or CDK inhibitors. The gene discussed is CCND1; the disease is breast carcinoma.