This study additionally indicated that the relative rarity of symptomatic patients with IL-12RB2 deficiency relative to IL-12RB1 deficiency was not because of differences in the frequency of the genetic disorders, but due to lower clinical penetrance: the isolated absence of IL-12RB2 was, at least in part, compensated by other cytokines for the production of IFN-γ, which thereby provided some protection against mycobacteria. Here, IFNG is linked to hereditary disease.