Cells from the Eμ-PRMT5/TCL1 model again featured a gene expression signature that is concordant with RT tumors and the Eμ-PRMT5 model, where dysregulated PRMT5 and upregulation of genes including Ctla4, Cd274 (Pd-L1), and Il-10 suggest aberrant activation of PRMT5 in B lymphocytes predisposed to CLL may further manipulate the surrounding environment to facilitate tumorigenic outgrowth in secondary lymphoid niches. Here, CTLA4 is linked to B-cell chronic lymphocytic leukemia.