In line, recent findings on resistance of AML cells e.g., upon exposure to a multikinase inhibitor targeting fms such as tyrosine kinase 3 (FLT3) as well as IL-1 receptor-associated kinase 1 and 4 (IRAK1/4) point to a mechanism associated with NF-κB [50]. This evidence concerns the gene CSF1R and acute myeloid leukemia.