Dysregulated STAT3 activation leads to VEGF overproduction and increased angiogenic phenotype in GC [143]. c-Myc, which is overexpressed after Helicobacter infection, is a STAT3 target gene and can compensate for the role of STAT3, contributing to gastric epithelial cell proliferation [144]. This evidence concerns the gene MYC and Helicobacter pylori infectious disease.