Activation of type I interferon signaling provides an alternative pathway to the upregulation of MHC-I expression in IFNγ-resistant tumor cells [63,79,216], via treatments such as cGAMP (2′3′ cyclic guanosine monophosphate-adenosine monophosphate) and BO-112 (a nanoplexed version of polyinosinic:polycytidylic acid) that activate innate interferon sensing in tumor cells in the NLRC5- and IFNγ- independent manner [63,78]. The gene discussed is IFNG; the disease is neoplasm.