A combination of the DNMT inhibitor 5AZADC and ADU‐S100 restored the tumor‐cell intrinsic STING signaling defect due to epigenetic programming and enhanced the anti‐tumor response against melanoma in vivo.[50] For CINhigh tumors, the STING inhibitor C‐176 led to the downregulation of pathways related to inflammation, EMT, and ER stress and prolonged the survival of CINhigh tumor‐bearing mice.[34] Using tocilizumab, blocking the IL‐6 receptor, the IL‐6 mediated immune suppression was prevented. The gene discussed is STING1; the disease is neoplasm.