In the KIT-independent GIST62, the screening of drugs demonstrated that bortezomib treatment resulted in anti-tumor effects through degradation of cyclin D1 and induction of checkpoint p53 and p21 (Figure 1), indicating that targeting of cyclin D1 by bortezomib inhibits KIT-independent GIST cell growth. This evidence concerns the gene KIT and gastrointestinal stromal tumor.