Mice in which bone marrow dendritic cells (BMDCs) were GBA1-deficient leading to the accumulation of β-GlcCer exhibited enhanced inflammatory responses suggesting that the inflammation-based pathologies of Gaucher’s disease arise from Mincle-mediated processes; this was supported by the observation that no such augmentation was observed in GBA1−/− × Mincle−/− BMDCs. This evidence concerns the gene GBA1 and Gaucher disease.