The observation that mutated UNG genes in B cells from patients with the hyper-IgM syndrome produce proteins deficient in uracil excision from ssDNA but not dsDNA (37) may also relate to our finding that the incision activity of hUNG fully applies to uracil in ssDNA (Figure 1E)—the direct product of AID in CSR (and SHM). This evidence concerns the gene UNG and hyper-IgM syndrome.