Interestingly, B1R activation contributes to demyelination in multiple sclerosis, while B1R inhibition or its genetic deletion decrease the neuroinflammatory response and myelin loss in the spinal cord (Dutra et al., 2011) and the upstream kininogen was established as a key mediator of neurodegeneration (Langhauser et al., 2012). The gene discussed is KNG1; the disease is multiple sclerosis.