This was corroborated in MPS IIIA x IL-1R1−/− mice, lacking the IL-1R1 receptor, which also resulted in reduced brain glial activation, reversal of working memory deficits and normalisation of hyperactivity, ultimately indicating IL-1 as a key effector of neuroinflammation in MPS IIIA disease (Parker et al, 2020). Here, IL1B is linked to mucopolysaccharidosis type 3A.