AKT1 and neoplasm: The drug’s antitumor activity is thought to arise primarily through inhibition of mitochondrial complex I, resulting in energetic stress and subsequent activation of AMP-activated protein kinase, which in turn downregulates the Phosphoinositide 3-kinase/Protein Kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) axis, a central pathway in tumour growth and metabolism [31].