Expanding the repertoire of non‐nucleotide STING agonists, SR‐717 has emerged as a promising candidate with potential for both systemic and oral administration, thereby enhancing the therapeutic options available for STING‐based cancer immunotherapy.[29] Mechanistically, SR‐717 activates STING in a manner similar to CDNs, wherein two SR‐717 molecules bind at the base of the intersubunit cleft of the STING dimer, triggering a closed lid conformation similar to the binding mode of 2′3’‐cGAMP. The gene discussed is STING1; the disease is cancer.