Specifically, astrocytes derived from PD patients carrying mutations in leucine-rich repeat kinase 2 (LRRK2) display significantly increased basal and compensatory glycolytic activity compared to controls [28], and LRRK2 PD astrocytes produce higher levels of IL-6 than control astrocytes after exposure to tumor necrosis factor (TNF) and interleukin-1 beta (IL-1β) [29]. The gene discussed is IL1B; the disease is Parkinson disease.