ABL1 and plasma cell myeloma: Metabolomic analysis has shown that BCR-ABL-ERK signaling drives the PPP and RNA biosynthesis in myeloma cells and that imatinib inhibits glycolysis and PPP uptake of glucose via acetyl coenzyme A and NADPH resulting in PPP damage and RNA nucleotide accumulation and negative regulation of mRNA.[46] Furthermore, Bone destruction is also a feature of myeloma, and osteoclasts are dependent on glucose metabolism on glycolysis and oxidative phosphorylation (OXPHOS), playing a key role in lactic acid production[47] (Fig. 4).