For example, one recent study reported that T-2 toxin, a mycotoxin that may potentially lead to the progression of AD, stimulates HIF-1α expression, along with induction of APP and hyperphosphorylation of tau proteins in microglial BV2 cells; intriguingly, further studies revealed that the T2-induced HIF-1α actually functions as a “brake” to negatively regulate APP induction and tau phosphorylation, suggesting a protective effect of HIF-1α in microglial cells challenged with T-2 toxin, in part by suppressing tau hyperphosphorylation [196]. The gene discussed is APP; the disease is Alzheimer disease.