The overexpression of PRMT5 in the fibroblasts and endothelial cells of SSc has provided the rationale that PRMT5 might be related to the fibroblast activation and endothelial dysfunction, which have been revealed as crucial in the pathogenesis of SSc.2 4 PRMTs have been shown to play critical roles in disease through methylation of arginine residues on histone or non-histone proteins. This evidence concerns the gene H2BC12L and endothelial dysfunction.