We are now more than 4 months into the peak of the COVID-19 pandemic with >5,000,000 infections and >330,000 deaths steadily increasingly worldwide, and although various respiratory and cardiac complications have been reported, we have not yet seen COVID-19–related neuroinflammatory or neuroautoimmune diseases as with the other viral outbreaks, including with coronaviruses MERS-CoV and SARS-CoV, which have 75–80% identical viral genome sequence with COVID-19.4 Whether this is due to COVID-19–inducing severe respiratory compromise soon after the median 4-day incubation period5 and underrecognition of neurologic events owing to overwhelming urgency to focus on life-saving efforts is unclear. In the most up-to-date large published series, apart from multifactorial acute cerebrovascular events in 5.7% of patients, the main COVID-19–related neurologic symptoms have been hypogeusia (in 5.6%), hyposmia (5.1%), and very high creatine kinase (CK) levels, with myalgia (in 19.3%) indicating potential CNS, peripheral nervous system, and myopathic manifestations.6 Things are however rapidly changing as just only the last 4 weeks the first COVID-19–triggered neurologic events are reported with at least 11 cases of GBS, the prototypic viral-triggered autoimmune neurologic disease, observed in the 4 main COVID-19 hotspots, Wuhan, Italy, Spain, and now France.7–11 The cases are of special neuroimmunologic and practical interest while highlight what is more to come.