BCL11A and Schnyder corneal dystrophy: The more efficient and less error-prone in silico methodologies revealed that rs61742690, which involved an S783N amino acid change in the zinc-finger domain of BCL11A, is an appropriate target for disrupting the BCL11A-mediated foetal-to-adult globin switch to continue the production of the HbF in SCD and β-thalassemia patients.