We have recently reported that HCV exploits the immunity-related GTPase M (IRGM), previously identified as a risk factor for Crohn’s disease and tuberculosis and for its role in autophagy (9) to regulate the activity of the vesicular transport protein GBF1 and of the small Arf1 GTPase (10), thereby leading to Golgi fragmentation and facilitating HCV replication through lipid supply (11). This evidence concerns the gene IRGM and Crohn disease.