Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Q: Restless legs syndrome (RLS), recently renamed Willis-Ekbom disease (WED), is a common movement disorder. It is characterised by the need to move mainly the legs due to uncomfortable, sometimes painful sensations in the legs, which have a diurnal variation and a release with movement. Management is complex. First, centres should establish the severity of RLS using a simple 10-item RLS severity rating scale (IRLS). They should also exclude secondary causes, in particular ensuring normal iron levels. Mild cases can be managed by lifestyle changes, but patients with a IRLS score above 15 usually require pharmacological treatment. Dopaminergic therapies remain the mainstay of medical therapies, with recent evidence suggesting opioids may be particularly effective. This article focuses on the different treatment strategies in RLS, their associated complications and ways to manage them.

A: Willis-Ekbom disease is also known as?
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Q: A significant role for IFN in the pathogenesis of systemic lupus erythematosus is well supported, and clinical trials of anti-IFN monoclonal antibodies are in progress in this disease. In other autoimmune diseases characterized by substantial inflammation and tissue destruction, the role of type I interferons is less clear. Gene expression analysis of peripheral blood cells from patients with rheumatoid arthritis and multiple sclerosis demonstrate an interferon signature similar to but less intense than that seen in patients with lupus. In both of those diseases, presence of the interferon signature has been associated with more significant clinical manifestations. At the same time, evidence supports an anti-inflammatory and beneficial role of IFN locally in the joints of patients with rheumatoid arthritis and in murine arthritis models, and many patients with multiple sclerosis show a clinical response to recombinant IFN. As can also be proposed for type I diabetes mellitus, type I interferon appears to contribute to the development of autoimmunity and disease progression in multiple autoimmune diseases, while maintaining some capacity to control established disease - particularly at local sites of inflammation. Recent studies in both rheumatoid arthritis and multiple sclerosis suggest that quantification of type I interferon activity or target gene expression might be informative in predicting responses to distinct classes of therapeutic agents.

A: Which is the most common gene signature in Rheumatoid Arthritis patients?
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Q: McLeod syndrome is caused by mutations of XK, an X-chromosomal gene of unknown function. Originally defined as a peculiar Kell blood group variant, the disease affects multiple organs, including the nervous system, but is certainly underdiagnosed. We analyzed the mutations and clinical findings of 22 affected men, aged 27 to 72 years. Fifteen different XK mutations were found, nine of which were novel, including the one of the eponymous case McLeod. Their common result is predicted absence or truncation of the XK protein. All patients showed elevated levels of muscle creatine phosphokinase, but clinical myopathy was less common. A peripheral neuropathy with areflexia was found in all but 2 patients. The central nervous system was affected in 15 patients, as obvious from the occurrence of seizures, cognitive impairment, psychopathology, and choreatic movements. Neuroimaging emphasized the particular involvement of the basal ganglia, which was also detected in 1 asymptomatic young patient. Most features develop with age, mainly after the fourth decade. The resemblance of McLeod syndrome with Huntington's disease and with autosomal recessive chorea-acanthocytosis suggests that the corresponding proteins--XK, huntingtin, and chorein--might belong to a common pathway, the dysfunction of which causes degeneration of the basal ganglia.

A:
Mutation of which gene is associated with McLeod syndrome?
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