Moreover, a second group took advantage of the “humanized” NOD/scid IL-2Rγ−/−/SGM3 (NSG/SGM3) mouse model, which combines a profoundly immune-compromised background with transgenic expression of the recombinant human growth factors SCF; granulocyte macrophage colony-stimulating factor (GM-CSF); interleukin-3 (IL-3), in order to facilitate robust engraftment of FA patient AML cells [55]. Here, CSF2 is linked to Friedreich ataxia.