Since then, studies have shown that the overexpression of PKC drives tumor development via synergistic activation of several cell-survival and mitotic pathways, including nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (Stat3), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), and extracellular signal-regulated kinase (ERK) [151,152]. This evidence concerns the gene AKT1 and neoplasm.