In addition, the enhanced entry of glucose carbon into the PPP, induced by oncogenic K-RAS and favored by negative HBP regulation of phosphofructokinase 1 (PFK1) through O-glycosylation [72], provides substrates for DNA and RNA synthesis under normal conditions of tumor growth and upon chemoresistance onset [73,74,75], reducing the importance of increased NADPH, which is necessary for the synthesis of fatty acids and glutathione (GSH), as well as for cell redox homeostasis [76]. Here, KRAS is linked to neoplasm.