From the 1940s, when chemist Linus Pauling defined the molecular basis of sickle cell anemia as the first molecular disease191, to Kan and Dozy in the 1970s defining the presence of single-nucleotide polymorphisms for the first time in the human genome in their paper entitled: ‘Polymorphism of DNA Sequence Adjacent to the Human Beta-Globin Structural Gene: Relationship to Sickle Mutation’192, to now the recent advance of gene-therapy strategies for SCD in present day193. This evidence concerns the gene HBB and Schnyder corneal dystrophy.