Although animal model studies indicate that FBP provides negative feedback that limits weight gain [24], which, given the observed negative association between BMI and GCA [6–8], would argue for it as a biomarker of increased GCA risk, it may also be that FBP1 activity, leading to increased availability of pyruvate, downregulates PD-L1 in macrophages, a pathway that would be protective against GCA [10, 12]. This evidence concerns the gene FBP1 and temporal arteritis.