Consistent with being an activator for NLRP3 activation, ATP’s expression profile was similar to the level changes of NLRP3, suggesting the contribution of released ATP (might be the potential priming signal) to NLRP3 activation in liver after HSCT, leading to NRLP3 inflammasome assembly, caspase-1 activation and release of IL-1β and IL-18, which promoted an inflammatory response and infiltration of neutrophils and macrophages into liver, resulting in liver inflammatory injury, similarly to the pathogenesis and development of GVHD. Here, IL1B is linked to graft versus host disease.