Moreover, inhibitors of symmetric (PRMT5-mediated) or asymmetric (type I PRMT-mediated) arginine methylation were also observed to preferentially kill serine and arginine-rich splicing factor 2 (SRSF2)-mutant leukaemia cells both in vitro and in vivo, and the mechanistic basis for this response in part reflects the observation that PRMTs predominantly target RBPs with established roles in splicing regulation [147]. The gene discussed is SRSF2; the disease is leukemia.