The small molecule Axl inhibitor BGB324 inhibits Akt and Erk signal transduction pathways. (A) Silencing of Axl with shRNA reduced sensitivity toward 3 µM BGB324 as shown by WST-1 assay of control-infected and shAxl-infected MV4-11 cells. Percentage of viable cells was normalized to untreated control cells (n = 3; *P < .05). (B) The effects of BGB324 on Axl overexpressing MV4-11 cells were more pronounced compared with control-infected cells (n = 3; *P < .05). (C) Immunoblot indicated inhibition of starvation-induced Akt phosphorylation in Gas6⁺ MV4-11 cells upon treatment with BGB324. Densitometric quantification of (pAkt/β-actin)/(tAkt/β-actin) was normalized to NM cells (n = 3; *P < .05). (D) BGB324 inhibited phosphorylation of Erk upon serum starvation as shown by immunoblot. Densitometric quantification of (pErk/β-actin)/(tErk/β-actin) was normalized to untreated cells (n = 3; *P < .05). (E) Immunoblot showing no inhibition of starvation-induced Akt phosphorylation by BGB324 in Gas6⁻ HL60 cells. Densitometric quantification of (pAxl/β-actin)/(tAxl/β-actin) was normalized to cells in NM (n = 3; *P < .05). (F) Inhibitory effect of 2 µM BGB324 on growth of Gas6⁺ OCI-AML5 cells was abrogated by Gas6 neutralization via sAxl (n = 3; *P < .05). (G) Expression of Gas6 rendered Gas6⁻ HL60 cells sensitive toward treatment with BGB324 (data normalized to untreated cells; n = 3; *P < .05). (H) Cytarabine (AraC; 4 µM) and BGB324 (2 µM) exerted additive inhibitory effects on MV4-11 cells (n = 3; *P < .05; #P < .05).