The prevalence of memory on the naïve NK-cell% could be accounted for by two IFN-γ-regulated facts: the promotion of CD4+ and CD8+ naïve to memory differentiation by a persistent secondary adaptive immune response, typical of SCD-related immune-dysregulation [28]; and the suppression of CD4+ follicular type 1 helper T cells, leading to a delayed germinal center response with a subsequent predominance of naïve on memory B-cell% and a paucity of activated CD21low B-cell% [29]. This evidence concerns the gene CD8A and Schnyder corneal dystrophy.