A study using mouse bone marrow progenitor cells co‐expressing NUP98::NSD1 and FLT3‐ITD reported that these cells are more sensitive to midostaurin compared to cells expressing either aberration alone, highlighting the defining role of the FLT3 signaling pathway in NUP98::NSD1‐driven AML.174. The gene discussed is FLT3; the disease is acute myeloid leukemia.