They found that MH treatment could play a key role in down-regulating DNMT1 and DNMT3B in prostate cancer cells, but not DNMT3A, via the ubiquitin-proteasome mechanism, particularly, the inactivation of Akt that mediates demethylation of the RASSF1A promoter. This evidence concerns the gene RASSF1 and prostate carcinoma.