Any deficiencies in IFN-γ, JAK1/2, or STATs including gene mutations, loss of protein expression, negative regulator presence, or epigenetic silencing would prevent signaling in response to IFN-γ and thereby end up to the up-regulated tumor growth and apoptosis inhibition and down-regulated T-cell infiltration and expression of PD-L1 and MHC-I (74, 78, 85, 86). The gene discussed is IFNG; the disease is neoplasm.