Studies have reported that DNMT1 gene expression was controlled via transcription factor Fli-1 in erythroleukemia cells [13], that DNMT1 expression was increased through the JAK-STAT pathway in malignant T lymphocytes [36], and that AKT activity inhibited DNMT1 degradation in multiple cell lines [37]. This evidence concerns the gene SOAT1 and erythroleukemia.