,92 Neuroinflammation and excessive Aβ deposition synergistically promote the development of AD,93 signal transducer and activator of transcription 3 (STAT3) mediates neuroinflammation and Aβ deposition in the process of AD, and the inhibition of CTSS in microglia can produce neuroprotective effects in AD.94, 95, 96 In mouse glial cells BV2, H2S reduces ATP-induced ROS production, inflammatory response, and Aβ1-42 deposition by eliminating phosphorylation of STAT3 and S-sulfhydration of CTSS at Cys25.97 This evidence concerns the gene STAT3 and Alzheimer disease.