We demonstrate that anemia, higher TGF-β1 levels, and AVWS are observed in older AS patients and LA100 mice, and the strong negative correlation between Hb and TGF-β1 and vWf multimers suggests that the anemia-induced increase in wall shear stress might be responsible for elevated activated TGF-β1 levels that then contribute to AS progression. The gene discussed is GSTM1; the disease is anemia (phenotype).