By designing and performing these simulations, we have demonstrated, for the first time, that introducing the SCD-causing mutation into the sheep HbB locus will create the propensity for polymerization of the beta Hb subunits, just as is seen in human patients with SCD, the very polymerization that is responsible for sickling of the RBCs. This evidence concerns the gene GSTM1 and Schnyder corneal dystrophy.