###### Abstract
Those CNVs can modify the genome structure and transposable elements within a region, thus affecting gene expression. They have been reported in healthy individuals [16; 17] and in different pathologies such as cancer or autoimmune diseases [14] they can also be used as diagnostic biomarkers in several diseases [16; 17]. Finally, CNVs seem to be involved in psoriasis pathogenesis through the modification of the expression of keratinocyte proteins involved in their cellular integrity and intercellular adhesion or its innate defense capacity, which would result in keratinocytes predisposed to induce psoriasis development [18; 19; 20; 21; 22]. The homozygous or heterozygous deletion of the late cornified envelope genes LCE3B and LCE3C is associated with an increase in the risk of psoriasis [18; 23]. An increment of \(\geq\)3 copies in the CNVs of CCL4/CCL4L is associated with psoriasis severity, whereas moderate disease correlated with a lower CNV (\(\leq\)2 copies); specifically, the CCL4L1 allele frequency is higher in severe psoriasis, whereas CCL4L2 is more frequent in patients with milder disease. CCL4/CCL4L genes encode for chemokines that stimulate T helper type 1 (Th1) cells, T regulatory (Treg) cells, monocytes, and dendritic cells (DC) [22]. On the other hand, the presence of certain CVNs has been associated with a better response to certain biological therapies, mainly anti-TNF [24; 25]. However, these studies have focused on the discovery of characteristic CNVs of psoriasis Vulgaris using blood samples and not the tissue that expresses the disease, which on many occasions presents in a focal manner on the elbows and knees or with the exclusive involvement of the scalp or palmoplantar area. Therefore, we consider that it might be more relevant to study whether there are common or differential CNVs between the different clinical phenotypes of psoriasis in the tissue that clinically expresses the disease. Apart from the above-related clinical types of psoriasis, anti-TNF drugs can induce the development of psoriasis recording [26; 27], of which PPP is the most frequent form of presentation [26; 27]. However, as the majority of patients receiving anti-TNF for inflammatory diseases other than psoriasis do not develop paradoxical psoriasis, some authors postulate that there must be an individual genetic background or unknown environmental factors that could predispose those patients since both the development and the latency period of paradoxical psoriasis is very variable [26; 27; 28; 29; 30]. In this regard, skin lesions derived from induced psoriasis present more plasmacytoid dendritic cells (pDCs), fewer T-cells, and selective overexpression of type I interferons, compared to classical psoriasis [31]. Anti-TNF drugs inhibit pDCs maturation, thus prolonging type I interferon expression. As a result, increased levels of type I interferon trigger the skin phenotype of paradoxical psoriasis in a T-cell-independent manner [32]. Thus, the aim of this study was to identify CNVs associated with the different clinical types of psoriasis that could explain the clinical-therapeutic differences found between them in clinical practice. As a secondary objective, we intended to assess the potential differences in genetic background between anti-TNF-induced PPP and the different clinical types of non-induced psoriasis, including psoriatic PPP.