Since quinacrine-induced cell death and mitochondrial depolarization were described to be mediated by MAPK-elicited BCL2 downregulation and suppressed by constitutively active MEK-1 over-expression (Changchien et al., 2015), we hypothesize that RAS pathway overactivation in t (6; 11)-r AML (Manara et al., 2014a) might prevent quinacrine-induced BCL-2 downregulation, thus avoiding synergy. The gene discussed is BCL2; the disease is acute myeloid leukemia.