Interconnected with IL-33, significantly attenuated and functionally defective ILC2s were found in triple transgenic AD mice (3xTg-AD), overexpressing amyloid, tau and presenilin-1, which also produced abnormally decreased amounts of protective IL-5 and developed pro-inflammatory gene expression of granzyme A, cathepsin A, and cathepsin H (Fung et al., 2021). The gene discussed is GZMA; the disease is Alzheimer disease.