 The study found that mutations in the TREX-1 gene, which encodes an exonuclease involved in DNA degradation, cause normocytic normochromic anemia in humans and mice. The authors demonstrated that TREX-1 dysfunction contributes to anemia by altering erythropoiesis and increasing the expression of erythropoietin and interferon-stimulated genes. This article was authored by Stephen L. Rigo, Scott Harvey, Sean R. Simpson, and others.