Treatment of lung cancer cells with actinomycin D and nutlin-3a primes cells for production of type I IFN by upregulating STING in a p53-dependent manner (Krześniak et al., 2020; Pu et al., 2021), suggesting a critical role of p53 in regulating STING levels to allow for type I IFN-mediated immune responses. This evidence concerns the gene STING1 and lung carcinoma.