A new immunotherapy candidate, STF-1623, developed by Stanford and Arc Institute researchers, inhibits ENPP1 to prevent degradation of cGAMP, a molecule activating the STING pathway in innate immunity. This drug demonstrates ultralong tumor retention with rapid systemic clearance, selectively restoring immune surveillance against tumors. Published in Cell Reports Medicine, STF-1623 represents a novel checkpoint blockade for ‘cold’ tumors resistant to existing immunotherapies.