The roles of the MAPK and NF‐kB pathways in fibrotic diseases have been widely reported.[41, 42] Among the NF‐kB transcription factor family, not only p65 but also the overexpressed cREL has been shown to regulate distinct transcriptional and functional profiles that drive fibroblast matrix production in SSc.[50, 51]. The gene discussed is NFKB1; the disease is systemic sclerosis.