There is strong association of PPARγ expression with the quiescent non-fibrogenic phenotype of HSC and a need to repress its transcription in order for the cells to adopt a myofibroblast phenotype.29, 30 We have previously shown that the methyl-CpG binding protein MeCP2 brings about this repression of PPARγ transcription at least in part by associating with methylated regions of the upstream promoter where it recruits chromatin remodelling factors.19 Hence, a higher degree of methylation at the PPARγ promoter would be expected to be a feature of fibrotic tissue in advanced liver disease. Here, PPARG is linked to liver disorder.