So far, the following cells and molecules have been identified to contribute to blister formation in experimental EBA: (i) cytokines including IL-1, IL-6, GM-CSF, CXCL1, and CXCL2, (ii) complement activation, (iii) adhesion molecules, such as beta-2 integrins, (iv) Fc gamma receptors, (v) neutrophil activation, and (vi) resolving of the inflammatory response. The gene discussed is IL1A; the disease is acquired epidermolysis bullosa.