Therapeutically inhibiting YAP1/TAZ signaling holds substantial promise. Yet the dual physiological roles of YAP1 in tissue repair and stemness underscore the need for highly selective and temporally controlled interventions. Rational combinations, such as pairing YAP1/TEAD inhibitors with immune checkpoint blockade, anti-fibrotic agents, may enhance clinical benefit. Future work should prioritize the development of robust biomarkers of YAP1 activation, deeper mapping of TEAD-dependent versus TEAD-independent functions, and optimization of strategies that maximize antitumor efficacy while limiting systemic toxicity.
Wu et al. (Thu,) studied this question.