Furthermore, this bradycardia is consistentwith data from patients taking mefloquine (which affects Cx36 GJs) for malariaprophylaxis (23); the fact that this drugcrosses the blood–brain barrier (24)may mean that the bradycardic effects observed are due at least in part to loss ofCx36-containing GJs, resulting in disrupted central sympathetic activity. The gene discussed is GJD2; the disease is Bradycardia.