AKT1 and gastric cancer: Importantly, clinical studies in gastric cancer patients human epidermal growth factor receptor HER2+ but non-responders to HER2-targeted therapy (including lapatinib) [54], showed that IGF1R and INSR contribute to the acquisition of the resistant phenotype by precluding the lapatinib-induced suppression of cell motility and apoptosis by re-stimulating both AKT1 and/or ERK signaling but also EMT-related signaling [55].