In addition, in a study performing gene expression profiling of SSc skin lesions followed by functional enrichment analysis, Inamo identified several pathways that were specifically upregulated according to the type of SSc autoantibody, namely “keratinocyte differentiation” pathways for ACA, “nuclear factor κB signaling” and “cellular response to TGFβ stimulus” pathways for ARA, “interferon α/β signaling” pathways for anti-U1 RNP, and “cellular response to stress” pathways for ATA [33]. This evidence concerns the gene TGFB1 and systemic sclerosis.