DEAR EDITOR, Epidermolysis bullosa (EB) is a heterogeneous group of inherited skin disorders characterized by blister formation. Classification of patients with EB begins with their separation into one of the four major EB groups, based on the level to which blisters develop: EB simplex (EBS), junctional EB (JEB), dystrophic EB (DEB) and Kindler syndrome. The next level of subclassification takes into account the clinical features present in a given patient, most notably the distribution and severity of cutaneous and extracutaneous disease involvement. 1,2We started DNA analysis of EB in 2005 when polymerase chain reaction (PCR) direct sequencing of COL7A1, KRT5 and KRT14 was introduced in connection with clinical, ultrastructural and immunohistochemical analysis. 3,4 In 2014, we implemented PCR direct sequencing of TGM5 and the solution-based capture method SeqCap EZ Choice Library (Roche NimbleGen; Roche, Basel, Switzerland) and targeted resequencing. A custom capture array was designed to capture exons and adjacent intron sequences of 83 genes associated with genodermatoses, of which 18 genes are associated with an EB phenotype [TGM5, PKP1, DSP, JUP (suprabasal EBS); KRT5, KRT14, PLEC, EXPH5, DST (basal EBS); COL17A1, LAMA3, LAMB3, LAMC2, ITGA6, ITGB4, ITGA3 (JEB); COL7A1 (DEB); and FERMT1 (Kindler syndrome)].