The high concentration of extracellular ATP in inflammatory lesions activates the purinergic P2RX7 receptor, which is expressed on immune and nonimmune cells of the gastrointestinal tract. The P2RX7 receptor participates in the initiation as well as the regulation of the inflammatory response and consequently can favor colon carcinogenesis. Using both genetic and pharmacological models of P2RX7 inactivation, we found that P2RX7 acted at an early stage to suppress the development of colitis-associated cancer. For details, see the article by Hofman and colleagues on page 835.