AKT1 and gastric cancer: In particular, aberrant activation of the phosphoinositol 3-kinase/protein kinase B (PI3K/AKT) pathway promotes the development of chemoresistance in a variety of tumor cells, including GC cells [18] by phosphorylating substrates via tyrosine kinase receptors, such as mTOR, GSK-3β, and JNK [19].