In the APP/PS1 mouse model of AD, Chi3l1 deletion contributes to a decreased amyloid plaque burden and increased peri-plaque expression of the microglial lysosomal marker CD68 at the transcriptional level, indicating that Chi3l1 may suppress glial phagocytic activation and promote amyloid accumulation [157]. The gene discussed is CHI3L1; the disease is amyloidosis.