We have shown that upregulation of UCP2 is an important mechanism for regulating ROS in AD-A LCLs in previous studies80,81, in ASD siblings with biomarkers of increased ROS81, and have now demonstrated that BT further increases the gene expression of UCP2 in all LCLs regardless of the type in this study, so BT may be enhancing this compensatory mechanism in the AD-A LCLs. The gene discussed is UCP2; the disease is Alzheimer disease.