Prior research has demonstrated that the alternative splicing of exon three in TREM2, a genetic risk factor for AD, is regulated by two paralogous RNA-binding proteins, CELF1 and CELF2, with CELF2 being implicated in the reduction of full-length TREM2 protein expression through exon three skipping and nonsense-mediated mRNA decay, which effects on microglial responses to the Aβ aggregation (Yanaizu et al., 2020). The gene discussed is CELF1; the disease is Alzheimer disease.