As noted above, we have found that CFMs attenuate cyclin B1 levels and promote G2M arrest in a variety of cancer cell types, and the fact that SFN caused G2M arrest in part by targeting Cyclin B1 it is likely that, similar to SFN, CFMs also stimulate G2M arrest in our parental and Everolimus-resistant RCC cells. The gene discussed is CCNB1; the disease is renal cell adenocarcinoma.