AKT1 and neoplasm: Further mechanistic insights have been demonstrated in HNSCC whereby quinacrine was able to restore the function of the tumor suppressive protein, tumor protein 53 (TP53), leading to enhanced capabilities of initiating apoptotic cell death following DNA damage with cisplatin chemotherapy [14]; Moreover, quinacrine treatment has been shown to suppress phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), mechanistic target of rapamycin (mTOR) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways [18].