In a mouse model of HSCT busulfan and cyclophosphamide (often used in transplant conditioning regimens) induced liver inflammation through NLRP3 activation, and the pharmacological inhibition of NLRP3 reduced infiltration of macrophages and neutrophils and improved liver function [53], thus suggesting that targeting NLRP3 may have a therapeutic potential to prevent transplant complications, particularly in the prophylaxis of liver inflammation after HSCT. The gene discussed is NLRP3; the disease is inflammation.