Beyond the classical ICD–DAMP axis and TME remodeling (summarized in Table 1), emerging molecular immune mechanisms further enhance the efficacy of OV therapy against malignant melanoma (Table 2): the cGAS–STING innate immune amplification mechanism is triggered by cytosolic dsDNA released during OV infection, leading to the production of chemokines such as CXCL10 and CCL5, forming an “interferon–chemokine” cascade. Here, STING1 is linked to infection.