Excess production and actions of reactive oxygen species (ROS) is a major trigger for the progression of molecular abnormalities that accompany many diseases. For example, cerebral ischemia-mediated surge of ROS induce misfolding and microaggregation of proteins resulting in protein dysfunction and toxicity in the affected areas. Timely removal of the ROS inducers and dysfunctional proteins may be an ideal strategy to prevent the complications caused by the ROS. A recent article published byLiu and colleagues demonstrated that ubiquilin-1 (Ubqln), an ubiquitin-like protein,prevents ROS mediated complications in cerebral ischemia. Ubqln mediated timely degradation of dysfunctional proteins is sought to mediate this protective effect.