Previously, it has implied the overexpression of Arg1‐mediated the limiting of the activity of inducible nitric oxide synthase may be a molecular mechanism underlying the hyperproliferation of psoriasis.[15] Lou et al. also demonstrates a rewiring of the urea‐metabolic pathway that results in increased Arg1, augmenting the release of polyamines that stabilize self‐antigen complexes, which further activate DCs.[13] However, some questions remain unsolved. This evidence concerns the gene NOS2 and psoriasis.