revealed that the RNA+polyamine+Hnrnpa1226‐237 complex[12] is considered as a self‐antigen, with aberrant polyamine metabolism driven by the overexpression of arginase‐1 (Arg1) in psoriatic keratinocytes enhancing the sensing of this complex by DCs.[13] Therefore, targeting metabolic and immunological disorders via eliminating psoriasis‐related self‐antigens could offer a synergistic strategy for psoriasis therapy.[14]. The gene discussed is ARG1; the disease is psoriasis.