In both the MV‐4‐11 xenograft model and a diffuse PDX model of FLT3‐ITD AML, the combination resulted in statistically significant tumour regression at clinically relevant doses of the compounds, with a delay in tumour regrowth at lower concentrations of MEN1703 and gilteritinib and minimal impact on tolerability. The gene discussed is FLT3; the disease is neoplasm.