Gastrointestinal stromal tumors (GISTs) are the most common malignant tumors in a type of gut tissue called mesenchyme. They’re caused by mutations that activate receptor tyrosine kinase (RTK) enzymes, and treatment with RTK inhibitors is initially successful, but over half of patients develop resistance, indicating a need for better treatments. Researchers recently investigated whether the drug THZ1, an inhibitor of the protein CDK7 that’s effective in other cancers, could help. They first confirmed that CDK7, which helps regulate the cell life cycle and gene transcription, was overexpressed in high-risk human GISTs. They also found that CDK7 overexpression predicted a poor outcome. However, low-dose THZ1 exerted pronounced anticancer effects in GIST cells both in vitro and in a mouse model. THZ1 also synergized with the RTK inhibitor imatinib to increase its efficacy. Specifically, THZ1 treatment reduced the transcription of c-KIT, one of the receptor tyrosine kinases that’s commonly activated in GISTs by downregulating the expression of OSR1, another dysregulated protein. Although further testing is needed, the results reveal CDK7 as a new predictive marker for GIST outcomes and suggest that combining RTK and CDK7 inhibitors is a promising strategy for GIST treatment.