However, in PD neuroinflammation-related studies, pro-inflammatory factors such as TNF-α, IL-1β, and IL-18 are significantly up-regulated in LPS/ATP-treated BV2 (a mouse microglial cell line), while knockdown of MALAT1 by sh-MALAT1 reverses the increased expression of these cytokines, suggesting that lncRNA MALAT1 can promote the occurrence of the inflammatory response by up-regulating inflammatory mediator expression (32). The gene discussed is IL1B; the disease is Parkinson disease.