Thus, we evaluated whether pharmacological inhibition of the pathways: (i) cell cycle control (using the pan-CDK inhibitor, Roscovitine), (ii) mTOR signaling (using the PI3K-mTOR inhibitor, BEZ235), (iii) eIF2 signaling (using the eIF2α inhibitor, Salubrinal) and (iv) 14-3-3 signaling (using BV-02) could be potentially exploited therapeutically in T-ALL in combination with Cn inhibitors such as CsA and/or other Cn specific inhibitors such as CN585 [16] or FK-506. This evidence concerns the gene EIF2A and acute lymphoblastic leukemia.