As a result, CagA binding molecules such as SRC, c-MET, CRK, SHP2, CRKL and GRB2 interacts with phosphorylated or non-phosphorylated CagA to stimulate downstream signals in the ERK activation inducing oncogenic effects on gastric cancer, whereas, CSK inhibits SRC family kinase functions and CagA-SHP2 signaling effects. Here, CSK is linked to gastric cancer.