Dnmt3b is also required postnatally in mice for fracture repair and angiogenesis [88], and human DNMT3B mutations are known to cause immunodeficiency, centromeric instability, and facial anomalies (ICF) syndrome [83], in which loss of DNMT3B activity results in DNA hypomethylation of the centromeric regions [89], as well as reduced interaction with the DNMT3L accessory protein [81]. The gene discussed is DNMT3B; the disease is ICF syndrome.