FLT3 and hematopoietic and lymphoid cell neoplasm: This phenomenon mirrors the extreme heterogeneity inherent to hematologic cancers—while FLT3 inhibitor combination strategies significantly improve survival in mutated patients, they concurrently drive resistance evolution through mechanisms such as kinase domain D835 mutations or RAS/MAPK bypass activation, providing unique models for mechanistic studies (Antar et al., 2020; Smith et al., 2015).