Thus, skin trauma, a trigger of the Koebner phenomenon of psoriasis, leads to the increase in IFNγ needed for KC activation.54 During wound healing, natural killer T cells (NKT cells) enter the wound and release IFNγ in early-wound infiltrates.55,56 Furthermore, colonization of the skin by SAg-producing S. aureus strains is associated with the severity of psoriasis vulgaris.57 In addition to these conditions found in psoriatic lesions, we mimicked, to some extent, the pathophysiological conditions of GvHD since we used alloreactive T cells in our coculture studies. The gene discussed is IFNG; the disease is psoriasis.