More recent studies have shown that NETs could contribute to the pathogenesis of psoriasis through a new mechanism independent of TLR7 or TLR9; this mechanism involves a crosstalk between TLR4 and IL-36R in psoriatic lesions, which could promote an inflammatory response, and highlight TLR4 as a possible new therapeutic target [154]. This evidence concerns the gene TLR4 and psoriasis.