Strengthening the hypothesis that SALL4-HDAC2 epigenetically repress transcriptional activity of invasiveness genes, knockdown of SALL4 leads to increased H3K27 acetylation and increased transcription of melanoma invasiveness-related genes, such as FN1, VEGFR-1, PDGFC, and NGFR, which could be partially rescued by administration of a histone acetyltransferase (HAT) inhibitor. The gene discussed is HDAC2; the disease is melanoma.