We propose that BAT activation, resulting in accelerated generation of lipoprotein remnants, should preferentially be combined with strategies that increase hepatic LDLR expression, including statins and/or proprotein convertase subtilisin/kexin type 9 blockers, thus fully unravelling the therapeutic potential of BAT for atherosclerosis prevention and treatment. The gene discussed is PCSK9; the disease is atherosclerosis.