Consistent with these observations, at present study we found that FGL2 silencing significantly inhibited ccRCC cells viability and ERK1/2 and p38 activation, and promoted cells apoptosis, suggesting that FGL2 aggravates the pathogenesis of ccRCC by promoting the activation of ERK1/2 and p38 MAPK signalling pathway. The gene discussed is MAPK3; the disease is nonpapillary renal cell carcinoma.