Our result with GRPR/NRG1 activation of HER4, mediating NSCLC cell growth via a MAPK-mediated mechanism, differs from studies that report that thrombopoietin [119], muscarinic M3 cholinergic receptor activation, and GRPR activation [120] stimulated transactivation of EGFR/HER1 in NSCLC cells, which mediated growth, invasion, or migration through a PI3K/AKT-dependent mechanism [121]. This evidence concerns the gene GRPR and non-small cell lung carcinoma.