While loss of DNA-PKcs or KU did not cause immediate bone marrow failture, expression of kinase-dead or phosphorylation defective (T2609A) DNA-PKcs compromised ribosomal RNA processing, protein translocation and hematopoiesis, and mice models with alanine substitution at all five (DNA-PKcs5A/5A) or three (DNA-PKcs3A/3A) out of the five threonine residues at the T2609 cluster succumbed to lethal anemia by 4 weeks [74, 187]. Here, PRKDC is linked to anemia (phenotype).