Other targets might be pathway-related proteins or co-occurring mutations, such as the NUP98::NSD1-associated FLT3-internal tandem duplication (FLT3-ITD), where inhibitors are part of current standard therapies, or, as has been recently shown, interferon signaling as a putative target pathway in FLT3-ITD-mutated NUP98::HOXD13 AML cell lines [1,75,76]. The gene discussed is NSD1; the disease is acute myeloid leukemia.