We demonstrated that TRPM2 deletion or knockdown: (1) reduced dopaminergic neuronal death; (2) prevented increases in microglial and CD68 density; (3) reversed microglial morphological alterations observed in the wild‐type PD animals; (4) decreased levels of pro‐inflammatory cytokines; (5) prevented CD68‐area increase in microglia; (6) alleviated cell death and improved cell viability in a neuron–microglia co‐culture; and (7) reduced phagocytosis and inflammation‐related molecules expression in microglia. This evidence concerns the gene CD68 and Parkinson disease.