Cancer cell responsiveness to type I and type II IFNs plays a role during immunoediting: cancer cells that eventually progress to form a tumor display reduced capacity to respond to IFN gamma, which otherwise would upregulate MHC class I molecules and render the tumors amenable to CD8+ T cell-mediated destruction, whereas responsiveness to type I interferon initially helps tumors avoid immune purging during the editing phase and is then irrelevant [81]. The gene discussed is IFNG; the disease is cancer.