Remarkably, we found that LSD1 demethylase activity is dispensable for maintenance of the pro-fibrotic gene expression in SSc fibroblasts, which was unexpected for two reasons: the heightened TGF-β signalling and the upregulation of the lncRNA HOTAIR, which localises chromatin-repressive modifier enzymes, including LSD1/coREST, to specific regions of the genome. This evidence concerns the gene RCOR1 and systemic sclerosis.