Foremost among controlling elements is the dominant role in directing tumor cell glucose utilization via protein phosphorylations supervised by the phosphoinositide 3-kinase (PI3K)/serine-threonine-specific protein kinase (Akt) —PI3K/Akt cascade—along with another serine-threonine kinase called “mammalian-target-of-rapamycin” (mTor) (Vander Heiden et al., 2010; Hanahan and Weinberg, 2011; Fruman and Rommel, 2014). This evidence concerns the gene MTOR and neoplasm.