Excessive erythrocytosis (EE) (Hb ≥21 g/dL in men, Hb ≥19 g/dL in women) is the main feature of CMS, and this excessive pathobiological response to hypoxia has deleterious effects, since a high hematocrit/hemoglobin increases blood viscosity and reduces blood flow to hypoxia-sensitive organs (e.g., brain and heart), often resulting in myocardial infarction, stroke, and high mortality in young adults (1, 3–7). This evidence concerns the gene GSTM1 and myocardial infarction.