Whereas the previous three mutations had profound impacts on T cell development, thereby explaining the resistance to ECM due to general T cell deficiency, in 2014 a genome-wide ENU mutagenesis screen identified a mutation in the gene Ccdc88b (coiled-coil domain containing protein 88b) that corelated with protection against cerebral malaria and had no bearing on thymic development (Kennedy et al., 2014). This evidence concerns the gene CCDC88B and congenital T-cell immunodeficiency.