Importantly, differential high-throughput drug screening of c.1380delA CDH1 SB.mhdgc-1 from HDGC patients versus sporadic gastric cancer cells identified increased sensitivity to EGFR inhibitors, including mTOR (Mammalian Target Of Rapamycin), MEK (Mitogen-Activated Protein Kinase), c-Src kinase, FAK (Focal Adhesion Kinase), PKC (Protein Kinase C) and TOPO2 (Topoisomerase II) inhibitors [116], suggesting that anti-mTOR, anti-PI3K and anti-EGFR therapies should be clinically trialed in HDGC patients. This evidence concerns the gene EGFR and Familial gastric cancer.