The type II protein arginine methyltransferase encoded by the PRMT9 gene serves as a regulator of alternative splicing.[18] PRMT9 upregulation has been reported in hepatocellular carcinoma tumors relative to healthy paracancerous tissue, with such overexpression being correlated with poorer tumor differentiation, vascular invasion, and more advanced Tumor Node Metastasis staging.[19] In protein interaction analyses, PRMT9 was predicted to interact with both PRMT5 and SF3B2. This evidence concerns the gene PRMT9 and neoplasm.