In a broader scope beyond sunitinib, accumulating evidence reported compensatory activation of PI3K/AKT/mTOR signaling pathway and/or heightened Mcl-1 expression in diverse cancer types resistant to other TKIs including imatinib, dasatinib, erlotinib, and gefitinib (Burchert et al., 2005; Wu et al., 2016). The gene discussed is MTOR; the disease is cancer.