The pharmacological inhibition of PRMT5 by 5′-methylthioadenisine (MTA) or the inhibition of PRMT5 using ShRNA increased RAS-ERK1/2 activity in response to hepatocyte growth factor (HGF) and resulted in tumor suppressive effects by downregulating EGFR and RAF1 signaling in PC12 tumor cells [94] (Figure 4). The gene discussed is HGF; the disease is neoplasm.