For example, the PROTAC exerted a significantly better activity against MV4-11 and wild-type MOLM-14 AML cells, but was less potent in OCI-AML3 cells, than the FLT-3 inhibitor, which is likely attributed to the extent of kinase engagement/selectivity of the PROTAC [10]. This evidence concerns the gene FLT3 and acute myeloid leukemia.