Elevated LRRK2 kinase activity promotes inflammatory responses, including activation of the inflammasome and NF-κB pathway, leading to increased secretion of pro-inflammatory cytokines (e.g., TNF-α and IL-1ß), which assist in pathogen clearance but also worsen colitis, chronic neuroinflammation, and dopaminergic neuronal loss in rodent models [171, 182, 186, 187]. This evidence concerns the gene LRRK2 and colitis.