When IFNγ is released from cytotoxic T cells, IFNγ binding to its receptor results in rapid and dramatic increased formation of the IFNγ receptor (IFNGR) heterotetrameric complex, which consists of IFNGR1 and IFNGR2, on the tumor cell membranes and subsequently initiates the JAK/STAT/IRF-1 signaling pathway21,22. The gene discussed is SOAT1; the disease is neoplasm.