NF‐κB activation drives the transcription of pro‐inflammatory mediators and immune‐regulatory genes in psoriasis, thereby contributing to sustained skin inflammation.[24] Our immunofluorescence staining validated the enhanced phosphorylation of NF‐κB p65 in psoriatic epidermis (Figure 3E), and FADS2 knockdown increased NF‐κB p65 phosphorylation in M5‐stimulated HaCaT cells (Figure 3F; Figure S2C, Supporting Information). The gene discussed is NFKB1; the disease is dermatitis.