The hypothesis that the CXXC5-Dvl PPI is a target for the development of drugs for the treatment of NASH was supported by the improvement in metabolic dysfunctions and pathological features of NASH with the restoration of the suppressed Wnt/β-catenin signaling target genes following KY19334 treatment. This evidence concerns the gene CXXC5 and metabolic dysfunction-associated steatohepatitis.