We previously showed that glycogen synthase kinase (GSK)-3β facilitates IFN-γ-activated STAT1 by inhibiting SHP2 [34], and aberrant PI3K and a decrease in PTEN increase AKT activation and GSK-3β inactivation to cause SHP2-activated IFN-γ resistance in gastric cancer AGS cells [35]. This evidence concerns the gene PTEN and gastric cancer.