The Axl inhibitor BGB324 inhibits survival of AML cells and induces sensitivity toward chemotherapy. (A) Axl-silencing in MV4-11 leukemia cells increased chemosensitivity of AML cells treated with 200 nM doxorubicin (Doxo). Percentage of viable cells was normalized to untreated control cells, respectively (n = 3; *P < .05). (B) Overexpression of Axl in MV-411 cells increased chemosensitivity of AML cells treated with 200 nM Doxo. Percentage of viable cells was normalized to untreated control cells, respectively (n = 3; *P < .05). (C) AraC (2 µM) and BGB324 (1 µM) elicited additive antileukemic effects in primary AML cells (n = 3; *P < .05; #P < .05). (D) BGB324 treatment reduced stroma-mediated resistance of HL60 cells toward treatment with AraC when HL60 cells were cocultured with S17 cells (n = 3; *P < .05; #P < .05). (E) Gas6-deficient HL60 cells were resistant toward treatment with BGB324 when stroma cells were absent. (F) In the presence of Gas6-producing murine stromal cells (OP9), HL60 cells became sensitive toward treatment with BGB324. Viable cell number was determined by WST-1 assay after 48 hours and normalized to untreated control cells without (E) or with (F) coculture (n = 3; *P < .05).