The NOD.Cg-Prkdc ^scid  Il2rg ^tm1Wjl /SzJ mice, most often known by their branded name, NOD scid gamma (NSG™), do not express the Prkdc gene nor the X-linked Il2rg gene.

NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.

The mice carry two mutations on the NOD/ShiLtJ genetic background; severe combined immune deficiency (scid) and a complete null allele of the IL2 receptor common gamma chain (IL2rg ^null).

The scid mutation is in the DNA repair complex protein Prkdc and renders the mice B and T cell deficient. The IL2rg ^null mutation prevents cytokine signaling through multiple receptors, leading to a deficiency in functional NK cells.

The immunodeficient NSG mice enable research in human immune function, infectious disease, diabetes, oncology, and stem cell biology.

These mice are resistant to lymphoma development even after sublethal irradiation treatment.

These mutant mice have been shown to readily support engraftment of human CD34⁺ hematopoietic stem cells, peripheral blood mononuclear cells (PBMC), patient-derived xenografts (PDX), or adult stem cells and tissues and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies.

NSG mice are highly sensitive to the diabetogenic effects of streptozotocin (STZ).