The article by Gelfand et al.1 is timely and interesting. A few queries came to mind regarding use of tumor necrosis factor (TNF)–α blockers in neuroimmunologic disorders: TNF-α blockers, such as lenercept, failed in multiple sclerosis (MS)2 and worsened the disease. Why do the authors think that infliximab, a TNF-α blocker, works in neurosarcoidosis? Infliximab can produce de novo demyelinating lesions that mimic MS. If it does, how would the authors differentiate those lesions as being secondary to the drug or from neurosarcoidosis? Since sarcoidosis presents with extracerebral manifestations of the disease in 90% of cases, how did lesions in the lung, for example, respond to infliximab use?