Yet, the outcomes of Artemis and PRKDC mutations at the cellular level are different, suggesting additional functions for DNA‐PKcs in V(D)J recombination.42 Artemis inactivation causes radiosensitive T‐cell and B‐cell SCID in humans, that is characterized not only by the absence of T and B lymphocytes but also by cellular hypersensitivity to ionizing radiation due to the inability to efficiently repair DSBs.43 Most Artemis mutations identified localize in the N‐terminal region of the protein and manifest with loss of nuclease activity. The gene discussed is PRKDC; the disease is severe combined immunodeficiency.