Further investigation showed the additive effects in imatinib-sensitive GIST-T1 and GIST882, and imatinib-resistant GIST430/654 and GIST48 via coordinated targeting of KIT (with imatinib) and CK2 (with CX4945/shRNA), evidencing inactivation of KIT and downstream intermediates AKT, mTOR and MAPK, cell viability, colony-formation assays, apoptosis, cell cycle analysis, wound healing and invasiveness (Figs. 3, 4; Supplementary Fig. 3). This evidence concerns the gene KIT and gastrointestinal stromal tumor.