Alternatively, based on the fact that c.242A>T of HOXD4 in the two leukemia patients is linked to a specific haplotype composed of three variants in other HOXD genes (c.746-79_746-68del and c.1025T>G in HOXD10 and c.557G>A in HOXD12), van Scherpenzeel Thim et al. speculated that the HOXD4 mutation is insufficient to confer leukemia susceptibility on its own, necessitating combined action of other HOXD variants.[10] In our patients, those HOXD variations and other HOX variants common to the two SEDAC subjects were not found. The gene discussed is HOXD4; the disease is leukemia.