Emerging evidence suggests that CHI3L1 contributes to amyloid plaque formation, as demonstrated by studies in APP/PS1 transgenic mice lacking CHI3L1, in which genetic deletion of CHI3L1 attenuated AD-like features, suppressed glial phagocytic responses, and reduces amyloid burden (Lananna et al., 2020). The gene discussed is APP; the disease is Alzheimer disease.