One informative next step will be to allow βS and β0-thalassaemia mutations to compete within the same interconnected network, alongside β+-thalassaemia mutations and other malaria-protective alleles with less severe clinical outcomes, for example HbC in Africa and HbE in Asia (Fucharoen and Weatherall, 2012, Piel et al., 2013). The gene discussed is KRT88P; the disease is thalassemia.