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The classical nonhomologous <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> end\u2010joining (<jats:styled-content style=\"fixed-case\">NHEJ<\/jats:styled-content>) pathway repairs double\u2010strand breaks in <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>. It is required for maturation of both B and T lymphocytes by supporting V(D)J recombination as well as B\u2010cell differentiation during class switch recombination (CSR). Inactivation of <jats:styled-content style=\"fixed-case\">NHEJ<\/jats:styled-content> factors Ku70, Ku80, <jats:styled-content style=\"fixed-case\">XRCC<\/jats:styled-content>4, <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> ligase 4, <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PK<\/jats:styled-content>cs, and Artemis impairs V(D)J recombination and blocks lymphocyte development. Paralogue of <jats:styled-content style=\"fixed-case\">XRCC<\/jats:styled-content>4 and <jats:styled-content style=\"fixed-case\">XLF<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">PAXX<\/jats:styled-content>) is an accessory <jats:styled-content style=\"fixed-case\">NHEJ<\/jats:styled-content> factor that has a significant impact on the repair of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> lesions induced by ionizing radiation in human, murine, and chicken cells. However, the role of <jats:styled-content style=\"fixed-case\">PAXX<\/jats:styled-content> during development is poorly understood. To determine the physiological role of <jats:styled-content style=\"fixed-case\">PAXX<\/jats:styled-content>, we deleted part of the <jats:italic>Paxx<\/jats:italic> promoter and the first two exons in mice. Further, we compared <jats:italic>Paxx<\/jats:italic>\u2010knockout mice with wild\u2010type (WT) and <jats:styled-content style=\"fixed-case\">NHEJ<\/jats:styled-content>\u2010deficient controls including <jats:italic>Ku80\u2010<\/jats:italic> and <jats:italic>Dna\u2010pkcs<\/jats:italic>\u2010null and severe combined immunodeficiency mice. Surprisingly, <jats:italic>Paxx<\/jats:italic>\u2010deficient mice were not distinguishable from the WT littermates; they were the same weight and size, fertility status, had normal spleen, thymus, and bone marrow. <jats:italic>Paxx<\/jats:italic>\u2010deficient mice had the same number of chromosomal and chromatid breaks as WT mice. Moreover, <jats:italic>Paxx<\/jats:italic>\u2010deficient primary B lymphocytes had the same level of CSR as lymphocytes isolated from WT mice. 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