The mutations in WT1 exon 7 in CTS and KASUMI-6 resembled common mutations in acute leukemia which lead to two presumed scenarios: either creation of truncated proteins with diminished or lost DNA binding capacity but intact 5′ transactivation, self-association and RNA-recognition domains or degradation by nonsense-mediated mRNA decay machinery and a possible subsequent haploinsufficiency. This evidence concerns the gene WT1 and acute leukemia.