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Seborrheic keratoses (SKs) are common benign nonmelanocytic epidermal tumors with characteristic clinical features, which are thought to allow a straightforward diagnosis in most situations. As a result, it is an accepted practice to destroy them without histopathologic confirmation. However, systematic reviews of histologic specimens reveal an erroneous clinical diagnosis or associated malignant tumors in a number of cases, including malignant melanomas. We describe a patient with a clinically typical-appearing SK, which was biopsied and histologically proven to be a malignant melanoma arising in the SK. Our report is a reminder that the reliability of clinical diagnosis of SKs needs to be questioned. In addition, a biopsy of SKs is not only warranted but necessary in order to identify a malignant melanoma that would otherwise be misdiagnosed or even completely missed.

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Additional information is available at the end of the chapter http://dx.doi.org/10.5772/54609 IntroductionEpidermolysis bullosa (EB) is a heterogeneous group of congenital disorders characterized by skin blister formation. EB is subdivided into three main subtypes (EB simplex (EBS), junctional EB (JEB) and dystrophic EB (DEB)) and one minor subtype (Kindler syndrome (KS)), according to the level of skin split [1].The EBS subtype can be defined as EBS with blisters within epidermal basal keratinocytes or above, and it is distinguished from other subtypes whose levels of blister formation are deeper (JEB and DEB) or variable (KS). Mutations in several genes have been identified as being responsible for EBS phenotypes. The clinical manifestations of EBS vary greatly depending on the causative genes. Some EBS subtypes are mild and tend to improve with age, whereas others are severe and often associated with early demise and/or other organ involvement. This chapter introduces the clinical and histological characteristics and classifications of EBS. Subsequently, each protein that is defective in EBS is discussed, as are animal models of the disease. Overview of epidermolysis bullosa simplexMutations in genes encoding keratinocyte components involved in the organization of the cytoskeleton or cell-cell junctions are responsible for EBS. EBS can be subclassified into basal and suprabasal according to the level of skin split [1,2] (Table 1).Basal EBS is caused by defects in skin basement membrane (BMZ) proteins. Figure 1 diagrams the skin BMZ. Among the BMZ components, keratin 5/14 and plectin are the main targets in EBS [3,4]. A few EBS cases have been reported to have mutations in ITGB4 and COL17, which encode 4 integrin and type XVII collagen, respectively [5,6]. Recently, BPAG1-e was added to the list of basal EBS target proteins [7,8].