Conversely, the comparison of cytokine expression in Il36rn−/− mice treated with Cl-amidine and untreated wild-type mice revealed differences in the IFN-γ and CXCL1 levels, and a completely similar recovery was not observed in the two groups, suggesting that the pathophysiology of contact dermatitis exacerbation in IL-36Ra knockout mice is not related solely to NETs. The gene discussed is CXCL1; the disease is contact dermatitis.