Recent studies have identified small molecules that can disrupt the binding of GAB2 to GRB2 (73, 74); additional studies will be required to determine whether blocking the interactions of GAB2 with its downstream partners, targeted GAB2 protein degradation, the inhibition of pathways downstream of GAB2, and/or other GAB2-targeting strategies may represent potential approaches for a variety of malignancies, including AML. This evidence concerns the gene GRB2 and acute myeloid leukemia.