As gain of function mutations in G protein subunit α q (GNAQ) have been previously speculated to drive tumor malignancy in melanoma and gastric cancer via activation of mitogen-activated protein kinase (MAPK) pathway [29, 30], we propose that genetic alteration of GNAQ renders tumor cells susceptible to ramucirumab treatment, the underlying molecular mechanism of which warrants further investigation. This evidence concerns the gene GNAQ and neoplasm.