This is because JAK1 mutations modulate the tumour immune microenvironment through the depletion of TILs, which results in IFN-γ insensitivity through epigenetic silencing of interferon-signalling components, or increased expression of negative regulators such as PD-1, TIM-3, CTLA-4, and LAG-3 [211,216,217]. The gene discussed is HAVCR2; the disease is neoplasm.