During hepatitis C virus infection, the Ub C-terminal hydrolase L5-mediated deubiquitination of NLRP3 enhances NLRP3 inflammasome activation in hepatocytes, underscoring its pivotal role in the pathogenesis of hepatitis C virus infection-induced liver diseases, including fibrosis, cirrhosis, and cancer [189]. This evidence concerns the gene NLRP3 and Cirrhosis.