In an in vitro BBB model with coxsackievirus A16 (CA16) infection and an in vivo CA16 infant rhesus monkey infection model, Song and colleagues suggested that CA16 infection downregulated miR-1303 levels and upregulated MMP9 expression, which promoted the degradation of junctional proteins, including claudin4, claudin5, VE-cadherin, and ZO-1, and ultimately causing neuroinflammation and injury to the CNS [188]. The gene discussed is TJP1; the disease is infection.