Previous studies have shown that SMCs in atherosclerotic plaques lose their contractile markers and acquire macrophage and fibroblast markers,14–17 preceded by differentiation into SEM cells15 or Lgals3+ SMCs.17 In vitro studies have shown that SMCs lose their markers and acquire macrophage and fibroblast markers secondary to cholesterol accumulation, which may be mediated by ER stress.14,24,25SMC-Abca1/Abcg1 deficiency increased accumulation of free cholesterol in bladder SMCs, whereas we could not detect CE (Figure 4A). The gene discussed is LGALS3; the disease is cholesteryl ester measurement.