We speculate that under limiting conditions, such as low doses of the STINGa ADC, low target expression on cancer cells, or lower frequency of FcγRI-expressing myeloid cells in the TME, which are expected to result in weaker induction of type I IFNs, type III IFN and possibly other factors/signals contributed by the cancer cell-intrinsic STING activation may provide a boost to increase the levels of type I IFN and ISGs, resulting in stronger anti-tumor innate immune activity. Here, STING1 is linked to cancer.