Here, the overexpression of the ASPG gene, codying for the enzyme asparaginase, promoted apoptosis resistance due to the increased production of asparagine and glutamate elicited by NRF2–ATF4 activation, while the AKT inhibition sensitized NSCLC tumors to L-asparaginase depletion from the extracellular space [98]. This evidence concerns the gene AKT1 and non-small cell lung carcinoma.