To maintain tissue homeostasis, apoptotic cells release factors that trigger the proliferation of surrounding cells. This process is known as 'compensatory proliferation' but is incompletely understood. As production of reactive oxygen species (ROS) is associated with apoptosis, the authors of this study proposed that ROS might trigger compensatory proliferation. They found that cells produce interleukin-11 (IL-11) in response to oxidative stress, but not in response to tumour necrosis factor or lipopolysaccharide. Oxidative stress induced the phosphorylation of the kinase ERK2 and the activation of the transcription factor FOS-related antigen 1, which promoted Il11 gene transcription. In a mouse model of acute liver injury, IL-11 was released by dying hepatocytes in a ROS-dependent manner and triggered the proliferation of neighbouring hepatocytes by activating STAT3. In the same model, treatment of mice with an IL-11 receptor agonist enhanced hepatocyte proliferation and reduced liver injury, whereas liver injury was exacerbated in mice deficient in the IL-11 receptor.