Plaque psoriasis is a chronic inflammatory skin disease affecting 1–3% of the general population causing a significant impairment of quality of life, particularly if diffuse and recalcitrant to treatments [
1]. Psoriasis is commonly associated with multiple comorbidities including psoriatic arthritis (PsA), inflammatory bowel diseases (Crohn’s disease and ulcerative colitis), cardio-metabolic disorders (such as myocardial infarction hypertension, obesity, diabetes, dyslipidemia, fatty liver disease, and hyperuricemia) [
2‐
5]. The association between psoriasis and cardio-metabolic comorbidities could be explained considering unhealthy life habits (i.e., smoking, over-eating, and sedentary life), the systemic nature of psoriasis-related inflammation, as well as common genetic and pathogenic pathways [
5,
6]. The current understanding of the psoriasis pathogenesis assigns central importance to an interaction between acquired and innate immunity [
7]. At the onset of the disease, plasmocytoid dendritic cells are activated in the dermis and produce tumor necrosis factor (TNF)-α and interleukin (IL)-23, which promote the development of T helper (Th)1 and Th17 lymphocytes which largely infiltrate psoriatic skin [
8]. Th17 cells are a recently identified cluster of differentiation (CD4)+ helper T cell subset which produce mainly IL-17A, IL-17F, IL-6, and, to a lesser extent, TNF-α and IL-22, which in turn are responsible for inflammatory changes and epidermal hyperplasia [
9]. Notably, TNF-α also synergizes with IL-17A to induce many psoriasis-related genes in human epidermal keratinocytes [
10]. IL-17A is produced not only by Th17 cells, but also by neutrophils, mast cells, and T cytotoxic cells. IL-17A promotes inflammation by several actions including: overexpression of antimicrobial peptides such as lipocalin2, human β-defensin 2 and S100A proteins; secretion of several CXCR1- or CXCR2-bearing neutrophil chemoattractants such as CXCL1, CXCL3, CXCL5, CXCL6, and CXCL8, leading to neutrophil accumulation in psoriatic epidermis; increased production of CCL20, which is essential for the recruitment of both CCR6-expressing dendritic cells and T cells in lesional skin; high expression of intercellular adhesion molecule-1 on endothelial cells, which is essential for T-cell extravasation; dominant role in inducing the expression of psoriasis signature genes that are synergistically or additively co-regulated together with TNF-α, including IL-19, a potent inducer of epidermal hyperplasia, IL-6 and IL-23A (IL-23p19) [
11‐
13]. Blocking IL-17A results in amelioration of psoriasis-like pathology in animal models [
14]. Secukinumab (Novartis Pharma AG, Basel, Switzerland) is a fully human IgG1κ monoclonal antibody (mAb) that selectively binds and neutralizes IL-17A. Here, we report the efficacy and safety results of phase II clinical trials that investigated the efficacy and safety of secukinumab in the therapy of chronic plaque psoriasis and PsA.