Figure 1 shows A, mutational frequencies of the four most commonly mutated splicing factors in hematological and solid tumors and B, schematic representation of the function of PRMTs in Sm-protein methylation and U1 U2 U4 U5 U6 spliceosome assembly. PRMT inhibition by small molecules lead to a reduction in U1 U2 and aberrant exon skipping and intron retention.