Based on recent publications suggesting that an amino-terminal portion of ASXL1 with dominant-negative or neomorphic activity could be expressed in some patients with hematologic malignancy (Asada et al., 2018; Balasubramani et al., 2015; Hsu et al., 2017; Inoue et al., 2016; Kitamura, 2018; Nagase et al., 2018; Yang et al., 2018), it will also be important in the future to produce zebrafish models that introduce asxl1 frame-shift mutations and premature termination in exon 11 or early in exon 12 to assess additional phenotypes that may accompany a truncated protein arising from this gene. This evidence concerns the gene ASXL1 and hematologic disorder.