AKT1 and Hyperglycemia: A successful example of biomarker-driven AKT therapeutics is the recent breakthrough by Craven et al. who showed that the mutant lysine in AKT1 E17K can be targeted by a covalent allosteric salicylaldehyde-based inhibitor that recruits endogenous Zn2+; by sparing collateral AKT2 inhibition, it is anticipated that this isoform-specific and mutant-selective inhibitor will result in decreased side effects, including hyperglycemia, in patients [448].