Glucose metabolism is indispensable to sustain Mcl-1 protein synthesis, and the inhibition of glucose metabolism results in a reduction of Mcl-1 levels, which helps to overcome Bcl-2 family inhibitor resistance, rationalizing the use of glucose metabolism targeted therapies in sensitizing cancer cells to apoptosis through the suppression of the expression of Mcl-1 [134]. This evidence concerns the gene BCL2 and cancer.