However, in 4T1 breast cancer tumors, the response to cGAMP was weaker, indicating a tumor‐type‐specific difference in STING pathway activation.[51, 56] In the B16‐F10 model, it was demonstrated that STING expression in non‐tumor cells was needed to mediate the anti‐tumor effect.[104] This emphasizes the role of the TME in responding to STING agonist treatment. This evidence concerns the gene STING1 and breast carcinoma.