In agreement with the role of sustained IFN-I signaling as a mechanism of resistance to PD-1 blockade in melanoma patients, the L. Zitvogel lab demonstrated that the activation of IFNAR1 signaling increases the expression of Nitric oxide synthase 2 (NOS2) on tumor cells and leucocytes cell fractions leading to intratumor accumulation of regulatory T cells and myeloid cells [16]. The gene discussed is IFNAR1; the disease is neoplasm.