performed a systematic longitudinal analysis of B‐cell subpopulations and corresponding immunoglobulin (Ig) levels to investigate the potential impact of B cells in psoriasis, finding the alteration of B‐cell subsets, particularly up‐regulation of transitional B cells (also known as TrB cells), short‐lived plasmablasts (PB), and IgA might be part of an inflammation‐induced compensatory mechanism in psoriasis. This evidence concerns the gene CD79A and psoriasis.