To further unravel the underlying mechanisms, Zhang et al. treated the imatinib-resistant GIST cell lines with PegIFNα2b, and showed that the combination of PegIFNα2b and imatinib, but not the PegIFNα2b alone, significantly inhibited cell proliferation and induced cell apoptosis by downregulating p-mTOR (phosphorylated mammalian target of rapamycin) and BCL-2 (B-cell lymphoma-2) [227], suggesting that the combination therapy has synergistic and imatinib-resistance reversing effects [227]. Here, MTOR is linked to gastrointestinal stromal tumor.