Similarly, anti-ICOSL treatment prevented the increased accumulation of Tfh cells in MZB cell–deficient Ldlr−/− mice and the acceleration of atherosclerosis.9 While Clement et al. 8 did not perform any characterization of the accumulated Tfh in their model, we showed that the accumulated Tfh cells in MZB-deficient mice were poorly differentiated.9 Thus, it was still unclear whether normal Tfh cell development in hyperlipidaemic mice was critical for atherosclerosis development. The gene discussed is LDLR; the disease is atherosclerosis.