Thus, to investigate the role of the NLRP3-caspase 1 pathway in HS pathogenesis, Kelly and colleagues found that caspase 1 activation was enhanced in HS skin and was associated with a higher expression (in HS lesional skin compared with healthy control samples) of both NLRP3 and IL-18 (a caspase 1-dependent pro-inflammatory cytokine) [111]. This evidence concerns the gene IL18 and histiocytic sarcoma.