Splice variants of PRMT2 bearing the SH3 domain and the cofactor-binding domain without an intact dimerization arm and beta-barrel domain (i.e., C-terminal truncations) have been implicated in breast cancer (55, 56).These variants were shown to be capable of augmenting estrogen receptor alpha–mediated transactivation activity. The gene discussed is PRMT2; the disease is breast carcinoma.