This leads to production of autoantibodies against Dsg1 and Dsg3, release of pro-inflammatory cytokines, and loss of cell-cell adhesion that ultimately results in the formation of blisters observed in PV.5, -7 While complement deposition may occur, it is not believed to be contributory to the pathogenesis of PV.8 This evidence concerns the gene DSG1 and acquired polycythemia vera.