Some results suggest that deletion of CD38 is neuroprotective, as decreased plaque loads and improved spatial learning are reported in Alzheimer's disease (AD) models (Blacher et al. 2015); however, contradictory reports of cognitive deficits (Kim et al. 2016) and increased susceptibility to infection (Lischke et al. 2013), which may be due in part to the ability of CD38 to regulate inflammation and the innate immune response (Partida‐Sanchez et al. 2001), are also found in Cd38 knockout mice. The gene discussed is CD38; the disease is Alzheimer disease.