CYSLTR1 and chronic myelogenous leukemia, BCR-ABL1 positive: A subsequent study revealed that montelukast, through a CysLT1R-dependent pathway, induced apoptosis of CML cells by inducing Bax overexpression, cytochrome C release, PARP-1 cleavage and caspase-3 activation, which could be additive to the pro-apoptotic effect of imatinib; montelukast also altered Wnt/β-catenin signaling, inducing phosphorylation of β-catenin and downregulating the downstream target c-myc [40].