We further establish that 2 stromal subtypes enriched in HS lesional skin, CXCL13+ and SFRP4+ FBs, play a major role in shaping and perpetuating the inflammatory response in HS through secretion of chemokines that recruit B cells and myeloid cells, as well as driving the extensive fibrosis that is characteristic of long-standing HS. This evidence concerns the gene CXCL13 and histiocytic sarcoma.