The endogenous heterozygous NRASG12D mutation was removed using CRISPR and a dox-inducible NRASG12V was introduced (B11 cells) to study the effects of NRAS mutations on self-renewal in human cells and compare them to our previous study of an MLL-AF9/NRASG12V murine AML [9]. The gene discussed is NRAS; the disease is acute myeloid leukemia.