Researchers observed that an influx of activated, mainly CD4+, HLA-DR+, IL-2 receptor-CD25+, T-cells was one of the earliest events of psoriasis.[21] Based on Mosmman and Coffman's publication,[22] these T-cells were classified as type 1 cytokine producers.[23] They produce interferon (IFN)-γ, IL-2, and tumor necrosis factor (TNF)-α cytokines and therefore implied that a cellular type 1 of reaction was responsible for psoriasis. The gene discussed is IFNA1; the disease is psoriasis.