While some of the observed activity profiles in CDH1-deficient cells, like select sensitivities to Src kinase in the CDH1(−/−) mutant MCF10A isoform, were in line with early signaling perturbations observed in T1a cancers of gastrectomy specimens of HDGC patients, other signaling aberrations observed in clinical specimens later in the transition of invasion beyond the gastric mucosa, like FAK and STAT3 kinase activation, were not found to be associated with select drug sensitivities in the MCF10A CDH1(−/−) in vitro system [10, 12]. This evidence concerns the gene PTK2 and Familial gastric cancer.