The mono-methylation of epidermal growth factor receptor (EGFR) R1175 by the PRMT5-MEP50 complex in breast cancer favorably controlled its trans-autophosphorylation at Tyr 1173, resulting in endogenous SHP1 recruitment to attenuate son of sevenless (SOS) phosphorylation and ERK activation (173). This evidence concerns the gene EGFR and breast cancer.