It has been reported that the overexpression of Erb-B2 Receptor Tyrosine Kinase 2 (ERBB2), mutations of EGFR/PI3K pathway, or the loss of Phosphatase and Tensin Homolog (PTEN), as well as mutations or amplification of AKT itself can result in increased PI3K-AKT signaling in tumor cells [26, 29]. The gene discussed is AKT1; the disease is neoplasm.