However, conflicting data came from another group documenting that the viability of AML cells and LSCs depends on LAIR-1 expression: LAIR-1 knockdown strongly enhanced AML cell line apoptosis and inhibited xenograft growth, and Lair-1-deficient MLL-AF9 and AML1-ETO9a induced murine AML models had a reduced LSC frequency and a longer survival. This evidence concerns the gene RUNX1 and acute myeloid leukemia.