In accordance with the results in the Cx32ΔTg-MCDD model, dysfunction of Cx32 accelerates NASH and fibrosis progression via an increase in reactive oxygen species (ROS), inflammatory cytokines, and activation of the brain expressed, X-linked 1 (Bex1)-NF-κB pathway (Sagawa et al. 2015). This evidence concerns the gene GJB1 and metabolic dysfunction-associated steatohepatitis.