PRMT5 and neoplasm: However, in breast cancer cells, abolishing PRMT5-mediated EGFR Arg1175 methylation increased EGF-induced extracellular signal-regulated kinase (ERK) activation by preventing the recruitment of Src homology 2 domain-containing protein tyrosine phosphatase (SHP)1 to EGFR, leading to enhanced cell proliferation, migration, and invasion of EGFR-overexpressing tumor cells [43].