For example, in an AD-related study, when a FYN kinase null mutant was crossed with the AD “triple transgenic” model (a mouse expressing mutated forms of APP, Tau, and PSEN1), male offspring were delayed in the development of Aβ pathology and spatial learning deficits, while female offspring showed no such temporal protection, i.e., decreased levels of FYN were protective only in males [54]. The gene discussed is APP; the disease is Alzheimer disease.