AKT1 and gastric cancer: To test whether the oncogenic function of PILRB was dependent on PI3K/AKT activation, PILRB-overexpressing GC cells were treated with GDC-0941 (a PI3K/AKT inhibitor), which inhibited AKT phosphorylation (Fig. 3D) and abolished the growth-promoting effect of PILRB expression, as determined by colony formation assays (Fig. 3E, F).