Since their discovery in the early 1990s, microRNAs (miRNAs), small, non-protein-coding RNAs with regulatory functions, have emerged from being a peculiarity in worms to abundant regulators of gene expression in nearly all organisms. There are more than 2500 miRNAs (miRBase 21, www.mirbase.org) in human, and the majority of proteincoding genes are thought to be regulated by miRNAs. Accordingly, miRNAs have been implicated in nearly all biological processes, in particular stem cell differentiation, development, the regulation of signalling pathways and defining cell identity.[1]Early studies with the ablation of all miRNAs by deleting Dicer, a key enzyme in the biogenesis of miRNAs, highlighted the role of miRNAs in skin development: mice with impaired biogenesis of miRNAs were not viable due to severe defects in skin structure.[2] Soon afterwards, individual miRNAs orchestrating epidermal differentiation and hair follicle development were identified, [3] and miRNAs were implicated in inflammatory and malignant skin diseases by identification of disease-specific miRNAs in psoriasis (s1), [4] atopic dermatitis (s2), delayed-type hypersensitivity reactions (s3), cutaneous T-cell lymphomas (s4), and basal (BCC) (s5) and squamous cell carcinomas (SCC) (s6, s7). Of particular interest, a miRNA with skin-restricted expression profile, miR-203, was identified (s8-s10) [4] , which regulates keratinocyte differentiation and proliferation and acts as a tumor suppressor.Psoriasis is a chronic inflammatory skin disease in which the disturbed interaction of keratinocytes and immune cells leads to a vicious circle of chronic inflammation. Are the deregulated miRNAs in psoriasis skin a cause or consequence of chronic skin inflammation? To answer this question, several
K E Y W O R D Sbiomarker, microRNA, non-coding RNA, psoriasis, skin