Given that a central facet of S. aureus virulence and manipulation of immune responses is its capacity to co-opt phagocytic programs, we postulate that AD pathobiology may involve altered phagosomal NOD2 activation by S. aureus. Thus, we sought to clarify NOD2-mediated modulation of type 2 T cell responses, more precisely whether innate NOD2 signaling may have the potential to counteract AD-like pathobiology. This evidence concerns the gene NOD2 and Alzheimer disease.