Upon tumor antigen recognition, T cells produce IFN-γ, which through the IFN-γ receptors (IFNGR1, IFNGR2), the Janus kinases (JAK1 and JAK2) and the signal transducers and activators of transcription (STATs) lead to antitumor effects, such as increased antigen presentation, transporters associated with antigen processing (TAP) and MHC, as well as increased production of chemokines [65]. The gene discussed is IFNG; the disease is neoplasm.