It was recently reported that p38 MAPK signaling and Dsg3 internalization play a pivotal role in pemphigus acantholysis (62); however, it has been also highlighted that blisters induced by monoclonal autoantibodies from PV patients are not affected by p38 or MK2 inhibition, indicating that this mechanism of blisters formation might be mainly related to steric hindrance (60, 61, 63). The gene discussed is DSG3; the disease is pemphigus.