Overlap of these genes cumulatively supports the notion that PRMT5 acts as a significant factor in evolution to RT and that RT tumors are highly active compared to classically indolent circulating CLL, where enrichment in mediators of cellular activity and cell cycle control (such as CCNA2, MYC) may be drivers of this phenotype. The gene discussed is MYC; the disease is B-cell chronic lymphocytic leukemia.