Blisters or macules are one of the clinical manifestations of erythema multiforme exudative. Erythema multiforme, also known as exudative erythema multiforme, is an acute inflammatory skin disease of complex etiology. The rash is polymorphic, often accompanied by mucosal damage, and its characteristic lesion is iris-like erythema. The disease occurs in spring and fall and is prone to recurrence. 10-30 years old has the highest incidence. Epidermolysis bullosa can be categorized into 3 main groups according to the level of blister formation under transmission electron microscopy. Mutations in different genes encoding proteins within the dermal-epidermal junction region provide the molecular basis for the different clinical presentations between subtypes. The level of epidermolysis bullosa in simple herpetic epidermolysis bullosa is at the basal cell layer and arises as a result of mutations in the basal cell keratin genes KRT5 and KRTl4. Tissue loosening in junctional epidermolysis bullosa occurs at the level of the zona pellucida of the dermal epidermal basement membrane as a result of ultrastructural evidence of abnormalities in the hemibridged granule-anchored filament complex, with specific mutations in the genes that encode three polypeptides, alpha;3, beta;3, and gamma;2, of the anchoring filament protein lamellipodial adherence protein 5 (1aminin). In addition, mutations in genes encoding components of hemibridged granules have been found in subtypes of junctional epidermolysis bullosa, including mutations in the gene encoding the alpha; 6beta; 4integrin beta; 4 subunit and mutations in the gene encoding the 18OkDa herpetic pemphigoid antigen BPAG2, also known as type VII collagen. Tissue loosening in dystrophic pemphigoid epidermolysis bullosa occurs at the level of anchoring protofibers under the dense zone, and only mutations in the type VII collagen gene (COL7A1) have been identified.