While the exact mechanism is not fully elucidated, one possibility is that the intestinal microbiota can either induce immune activation or trigger immune tolerance through cytokine stimulation.54 These changes, in turn, can exacerbate the T helper type 1 (Th1)/Th2 imbalance seen in AD, which is associated with increased secretion of IgE.55 Indeed, in vitro work demonstrated that a combination of non-specific strains of L. acidophilus, L. casei, L. reuteri, and B. bifidum (strains not specified) could exert anti-inflammatory properties through induction of T and B cell hyporesponsiveness.56 The gene discussed is IGHE; the disease is Alzheimer disease.