OTUB1 and infection: The deletion of Otub1 in T or B cells leads to immune cell hyperplasia and autoimmunity.14,15 Mice lacking Otub1 in astrocytes show severe central nervous system autoimmunity, and dendritic cell-specific deletion of Otub1 impairs the immune response of dendritic cells during infection and inflammation.16,17 Moreover, Ruiz-Serrano et al. reported that Otub1 knockout neonates died quickly after birth due to defects of lung development.18 However, the physiological roles and molecular mechanisms of OTUB1 in bone homeostasis remain unknown.