In AD, adaptive immune responses are mediated by CD8+ TEMRA cells, and EBNA3A and BZLF1 interact with TEMR to release pro-inflammatory interferon-γ (IFNγ), TNF-α, and cytotoxic factors (NKG7, GZMA, and B2M), leading to decreased cognitive function and further exacerbation of AD (Carbone et al., 2014; Gate et al., 2020; Kang and Liu, 2020; Tiwari et al., 2021). The gene discussed is B2M; the disease is Alzheimer disease.