H. pylori itself is known to induce double-stranded DNA damage in gastric epithelial cells [40–42], which when coupled with a BRCA1 or BRCA2 carrier’s elevated baseline gastric epithelial double-stranded DNA damage, may result in a synergistic increase in double-stranded DNA damage of the gastric epithelium and promote the development of GC. Here, BRCA1 is linked to gastric cancer.