Theoretically, longer FLT3-ITD has stronger phosphorylation signals and higher constitutive proliferative capacity regardless of the insertion site, reflected by less sensitivity to TKI when AML cell lines were exposed to quizartinib28, but this does not seem to be corroborated in the clinical experience, as shown in our analysis. The gene discussed is FLT3; the disease is acute myeloid leukemia.