In secondary brain injury using a rat intracerebral hemorrhage (ICH) model, it was observed that LRRK2 expression in the brain tissues after ICH had significantly increased, which in turn exacerbates the inflammatory response that is involved in secondary brain injury of ICH, thereby aggravating brain edema, blood–brain barrier damage, as well as cell death (33). Here, LRRK2 is linked to intracerebral hemorrhage.