Blocking IL-17A via a neutralizing antibody (secukinumab) reduced hyperkeratosis, acanthosis, and hyperproliferation, significantly decreased the levels of gene expression of chemokines derived from keratinocytes, such as CXCL1 (GRO) and CXCL8 (IL-8), and triggered near-total elimination of IL-17-positive epidermal neutrophils. The gene discussed is CXCL1; the disease is Hyperkeratosis.