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The pathogenesis of psoriasis has not been fully defined. The dysfunction of T cell subsets is considered to play a key role in the pathogenesis of psoriasis, and the biologics targeting T cell subsets have also become a milestone in the treatment of psoriasis. However, there are still some problems in the application of existing biologics, suggesting that the current understanding of the pathogenesis of psoriasis is still insufficient. There is increasing evidence that tumor necrosis factor-α-induced protein 3 (TNFAIP3), a negative feedback regulator of NF-κB, plays an important role in the pathogenesis of psoriasis through the regulation of T cells, keratinocytes, dendritic cells and other immune cells. In this review, the research progress of TNFAIP3 gene, its relationship with psoriasis and its mechanisms of action are reviewed, providing reference for the search for new therapeutic targets for psoriasis.