Moreover, we also found that OASL overexpression could upregulate TET1 in normal CD4+ T cells and that OASL silencing inhibited TET1 expression in CD4+ T cells of SSc patients, which suggests that OASL may play a pathogenic role in the activation of CD4+T cells in SSc through DNA hydroxymethylation mediated by TET1. The gene discussed is CD4; the disease is systemic sclerosis.