Studies found that when the SRC/FAK pathway was disturbed, FAK began to be depleted, and the isolation of FAK-high-efficiency cells or the expression of non-phosphorylated FAK proteins resulted in the active SRC to be isolated from focal adhesions into intracellular sites (48), and inhibition of autophagy recovered active SRC in the peripheral adhesion process to cause the death of cancer cells. This evidence concerns the gene PTK2 and cancer.