In a transgenic mouse model of AD, cathepsin X upregulation in microglial cells surrounding amyloid plaques has been observed, and further, the involvement of cathepsin X in amyloid-β-related neurodegeneration through proteolytic cleavage of the C-terminal end of γ-enolase has been suggested (Wendt et al., 2007; Hafner et al., 2013; Pislar and Kos, 2013). The gene discussed is CTSZ; the disease is Alzheimer disease.