We further showed that BETi-pazopanib synergy may be facilitated by the abrogation of BRD4-mediated control over MYC. Overall, our work supports the utility of phenotypic-driven drug discovery for personalized medicine and provides preclinical evidence for the further development of BETi-pazopanib as an alternative treatment option for STS. The gene discussed is MYC; the disease is telomere syndrome.