In another study, it was revealed that K685-acetylated STAT3 cooperates with DNMT1 to silence several tumor suppressor genes, including TP53, SHP-1, SOCS3 and CDKN2A, in melanomas; mutation of STAT3K685 or treatment with resveratrol (a histone deacetylase activator) was found to diminish the tumor-promoting function of STAT3 in melanoma [127]. This evidence concerns the gene CDKN2A and neoplasm.