Several of these mechanisms, such as mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) deficiency, fibroblast-specific inhibitor of nuclear factor kappa-beta subunit beta (Ikk2) deficiency, and Matt deficiency, have been only loosely correlated to human AD, and a clear understanding of their pathogenic contributions resulting in AD has yet to be fully delineated [2,3,4]. The gene discussed is MALT1; the disease is Alzheimer disease.