Levels of the transcriptional regulator IRF8 were significantly suppressed in monocytes from patients with diffuse cutaneous SSc and negatively correlated with the mRSS, and IRF8-silenced monocyte-derived macrophages displayed an M2 phenotype and significantly Along with upregulating the mRNA and protein levels of pro-fibrotic factors and extracellular matrix components, IRF8 silencing also exhibited a pro-fibrotic trend in a BLM-induced fibrosis mouse model [53]. This evidence concerns the gene IRF8 and fibrosis.