In conclusion, our studies demonstrated increased NLRP3 and caspase-1 activation in liver together with elevated release of ATP and HMGB1 were observed after conditioned by BU/CY during HSCT and inhibition of NLRP3 activation reduced inflammatory cell infiltration, ameliorated liver inflammation and improved liver function, suggesting therapeutically targeting it might be beneficial in the prophylaxis and treatment of liver inflammation after HSCT. The gene discussed is CASP1; the disease is Hepatitis.