Another consequence of an infection by HSV-1 is its capacity to produce the suppressor of cytokine signaling-3 (SOCS3), a host negative regulator of the JAK/STAT pathway, which, in turn, inhibits the IFN-γ capacity to induce phosphorylation of JAK kinases (Yokota et al., 2004). The gene discussed is IFNG; the disease is infection.