Recently, Lemos et al reported that STING-induced antitumor immunity can be transient and unstable due to STING responsive pathways, such as IDO and COX2, which act as negative regulators of antitumor immunity.30 31 To verify possible IDO and COX2 involvement as resistance mechanisms to STING treatment in the PCCC model, we assessed their expression and activity in peritoneal tumors and tumor-draining lymph nodes (TDLNs) following STING agonist treatment (figure 7C, D). Here, STING1 is linked to neoplasm.