Schematic depiction of myeloma dormancy as a reversible, dynamic state induced, in part, by binding of GAS6 on osteoblasts to the receptor tyrosine kinase, AXL, on mouse 5TGM1 myeloma cells. In this experimental model system of human myeloma, the reactivation of a miniscule fraction of dormant tumor cells suffices to generate bulk myeloma in the hematopoietic bone marrow (eg, as few as ∼15 cells account for the total tumor burden in long bones of untreated mice).⁵  New findings reported implicate the endosteal niche in a novel, environmentally induced phenotypic change in dormant myeloma cells that includes the ectopic expression of myeloid genes, such as Axl and Vcam1 (which partners with α4β1 integrin on osteoblasts; not shown). Additionally, Khoo et al demonstrate that dormant myeloma cells can be dislodged from survival-protecting niches using small-compound AXL inhibitors. Gilteritinib, an AXL-inhibiting drug that very recently won US Food and Drug Administration approval for the treatment of adult patients with acute myeloid leukemia that harbors mutated FLT3, may lend itself to evaluating this possibility in clinical trials of myeloma. In addition to promoting dormant myeloma cells, the interaction of AXL and GAS6 in the osteoblastic niche also governs dormancy of prostate cancer cells⁹  and survival and self-renewal of chronic myeloid leukemia stem cells.¹⁰  GAS6, growth arrest specific 6.