Nevertheless, T cell-specific KO of HDAC1 alone does cause an increased Th2-type inflammatory response in a mouse model of asthma, which is characterized by elevated expression of IL-4, IL-5, and IL-10, suggesting that HDAC1 represses cytokine production in activated T cells and during T effector (Teff) cell differentiation [56]. The gene discussed is HDAC1; the disease is asthma.