Indeed, showing that variants at SAR1a are not associated in HbF regulation at steady state in SCD patients could be consider interesting; the findings provide further evidence of the complex nature of Hb F regulation, highlighting that steady-state genetic regulators of γ-globin expression are not necessarily best suited targets for therapeutic interventions, therefore suggesting widening of the search for drug-responsive targets for HbF activation. This evidence concerns the gene GSTM1 and Schnyder corneal dystrophy.