In this regard, we observed that AML patients carrying NPM1 mutations showed a specific NIPBL downregulation and a zebrafish model with NIPBL haploinsufficiency presented defects in myeloid cell differentiation, demonstrating that animal models could enhance the comprehension of the action of multiple mutations/dysregulations (Mazzola et al., 2019). This evidence concerns the gene NPM1 and acute myeloid leukemia.