Other erythrocyte genetic abnormalities, such as α-thalassemia and glucose-6-phosphate dehydrogenase (G6PD) deficiency, can also confer protection against malaria  (Taylor et al., 2013; Kakande et al., 2020) and coexist in populations affected by HbS in malaria endemic areas. This evidence concerns the gene G6PD and thalassemia.