Our hypothesis was that the translocation of the examined leiomyoma had created a genomic breakpoint in intron 3 of KAT6B, similar to what was found in the four uterine leiomyomas reported by Moore et al. [15], one of which had a balanced t(10;17)(q22;q23) as the sole chromosomal abnormality. This evidence concerns the gene KAT6B and uterine corpus leiomyoma.