The rapid and robust improvement in psoriatic symptoms with interleukin (IL)‐17A‐targeting therapies including secukinumab, a fully human monoclonal anti‐IL‐17A antibody, enhanced the understanding of the pathogenesis of psoriasis (PsO).1, 2, 3, 4, 5 Evaluating gene expression in skin biopsy specimens from patients with PsO revealed a set of genes related to PsO, the expression of which changed following IL‐17A inhibitor therapy.6, 7 However, studies evaluating serum biomarkers in patients with PsO on IL‐17A inhibitor therapy are scarce.3, 5, 8, 9. This evidence concerns the gene IL17A and psoriasis.