Designing isoform-specific drugs having mutant or allele selectivity, such as inhibitors that target AKT1 E17K (https://www.rcsb.org/structure/8uw9), can potentially result in an even greater reduction in off-target effects, similar to drugs targeting the mutant form of PI3Kα, which delayed the onset of rash and hyperglycemia in patient-derived tumor xenograft models [421]. The gene discussed is AKT1; the disease is Hyperglycemia.