Thus, when aligning drug phenotypes derived from both in vitro models of HDGC, CDH1−/− null MCF10A and c.1380delA CDH1 HDGC cells, gastric cancer cells with defective CDH1 function showed selective overlapping sensitivity to PI3K, mTOR, ALK/ROS-1 like tyrosine, and aurora kinase inhibition in both systems. This evidence concerns the gene ALK and gastric cancer.