Because the activation of the LIF/STAT3/FGFR4 axis appears to function as a survival mechanism, promoting the growth of tumorigenic cells in response to aberrant expression of LIF and FGFR4 in the intestinal subtype of GC, our study supports the therapeutic potential of anti-LIF based therapies in the treatment of FGFR4 related settings in GC and potentially other neoplastic settings, such as colonic or hepatic tumors. The gene discussed is STAT3; the disease is gastric cancer.