Sharma et al. focused on the metabolic response to chemotherapeutic agent fludarabine: CLL cells, namely MEC-1 and 2 cell lines and primary samples showed an entirely similar profile to fludarabine resistant cells, a profound mTOR activation that caused an overall increase in glycolysis and OXPHOS rates, combined with an upregulation of purine biosynthesis [105]. This evidence concerns the gene MTOR and B-cell chronic lymphocytic leukemia.