Genetic mutation of FMS‐like tyrosine kinase‐3 (FLT3) is a target of interest for AML treatment, but the use of FLT3‐targeting agents on AML patients has so far resulted in poor overall clinical outcomes.[1] The incorporation of the boronic group in a drug scaffold could enhance the bioavailability and pharmacokinetic profile of conventional anticancer chemotypes. Here, FLT3 is linked to acute myeloid leukemia.