Furthermore, IAG933, a first-in-class direct disruptor of the YAP–TEAD interface, has shown rapid and potent suppression of TEAD-dependent transcription and robust anti-tumor effects across Hippo-dysregulated and KRAS- or MAPK-altered tumor models—including mesothelioma, NSCLC, and pancreatic ductal adenocarcinoma—and is also in phase I clinical trials [64]. This evidence concerns the gene KRAS and neoplasm.