As suggested elsewhere [27], [28], this is probably due to the occurrence of HSP, particularly HPE-type HSP, because (1) memory subsets, particularly the EMint/late subset, expressed the proliferation marker, Ki-67, at higher levels than the naïve subset, and the levels were much higher than those expressed by the EMint/late subset within human PBMC population; (2) the EMint/late subset showed the greatest IFN-γ-producing capacity; and (3) IL-2, IL-7, and IL-15 were undetectable in the plasma when CD4+ T cells converted to an activated memory phenotype. Here, IL2 is linked to holoprosencephaly.