“…Furthermore, we also explored the association of lncRNA NEAT1 expression with disease condition as well as inflammation level in patients with AIS, and we observed that lncRNA NEAT1 high expression was associated with increased NIHSS score, raised CRP level, elevated pro‐inflammatory cytokines levels (including TNF‐α, IL‐6, IL‐8, and IL‐22), and reduced anti‐inflammatory cytokine level (IL‐10) in patients with AIS. The possible reasons for these results might be as follows: (a) lncRNA NEAT1 might enhance the dysfunction of cerebral microglial cells through Wnt/β‐catenin signaling pathway, thus, it contributed to impairing the normal cerebrovascular physiology that led to advanced disease severity, and consequently, elevated NIHSS score was found in lncRNA NEAT1 high expression patients with AIS; (b) lncRNA NEAT1 might induce the loss of motor neurons and lead to the devastating neurodegenerative disorder, thus aggravated the abnormal cognitive deficits and functional activities of patients with AIS and increased the NIHSS score; (c) lncRNA NEAT1 promoted intima thickening or vascular occlusion by modulating the phenotype conversion of vascular smooth muscle cells, together with excessive apoptosis of epithelial cells, which might enhance the atherosclerotic lesion and aggravate the severity of AIS, thus lncRNA NEAT1 correlated with increased NIHSS score; (d) lncRNA NEAT1 might enhance the reactive oxygen species (ROS) level to disturb the normal initiation of inflammatory cascades, which further induced excess production of inflammatory cytokines, and thus, it led to increased levels of inflammatory factors (including CRP, TNF‐α, IL‐6, IL‐8, and IL‐22) as well as reduced anti‐inflammatory cytokine level in patients with AIS …”