In addition, the HMTs, SUV39H1, and WHSC1, were downregulated by IFN-γ or IL-4, at least in part, as a consequence of cell cycle arrest. Since SUV39H1 methylates H3K9 and places a repressive mark (62), it is predicted to reduce transcription of susceptible genes. Interestingly, one of the genes decreased by SUV39H1 in macrophages is p21waf1 (73), the cyclin-dependent kinase inhibitor that is responsible for inhibition of proliferation by IFN-γ or IL-4 (34, 35). Conversely, expression of p21waf1 indirectly downregulates SUV39H1, which implies a mutual feedback mechanism that presumably fine tunes the rate of proliferation. WHSC1 is a candidate gene implicated in Wolf-Hirschhorn syndrome, which is caused by deletions within the chromosome 4p16.3 region (74, 75). It has the ability to methylate several lysine residues in H3 and H4 (76) and could, therefore, act as a transcriptional activator or repressor. It has been ascribed a variety of functions, including in replicative DNA repair (33), which implies a role in S phase, but also in sustaining NF-κB pathway activity in tumors (77), which suggests activity may be present in other phases of the cell cycle. So far, there appears to be no knowledge regarding its role in macrophages.