MCL1 and neoplasm: B56δ is a regulatory subunit of phosphatase 2A (PP2A) while MET is reported to relieve PP2A inhibition by downregulating the expression of cancerous PP2A inhibitor.[35] Therefore, the combination of glucose depletion and MET is expected to enhance the PP2A expression and promote the dephosphorylation of downstream glycogen synthase kinase 3β (GSK3β), resulting in the inhibition of anti‐apoptotic MCL‐1 proteins and promoting tumor cell apoptosis (Figure 3B).