Furthermore, an autocrine loop has been identified in NSCLC, in which tumor-derived VEGF-A induces the secretion of VEGF-A itself and other proangiogenic factors, an effect mediated by the phosphatidylinositol-3-kinase (PI3K)/Protein Kinase B (AKT), RAS/extracellular signal-regulated kinase (ERK), and STAT3 signaling pathways [81]. The gene discussed is AKT1; the disease is neoplasm.