Furthermore, Saresella et al. (2014) demonstrated that Th17 cell activation occurred in AD patients and suggested that infiltration of Th17 cells into the brain played a role in the neuroinflammation and neurodegeneration of AD by proinflammatory cytokine release and by a direct action through the Fas/FasL apoptotic pathway (Zhang et al. 2013a, b). The gene discussed is FAS; the disease is Alzheimer disease.