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In conclusion, our study provides significant preclinical evidence that targeting the CDK4/6-DUB3 axis is an effective therapeutic strategy to destabilize YAP1 and suppress HCC progression

This is a hypothesis to be tested, not an assumption

Loss of FOXO3 leads to severe inactivation of Keap1, which in turn cannot prevent the activation of Nrf2, which is a very important finding in tumors

First, the risk profile of patients enrolled in the RCTs does not necessarily match that of patients for whom we are considering weighing the long-term benefits and potential harms

207 TGF- modulates angiogenesis through context-dependent effects, promoting VEGF, FGF, and PDGF expression while also inducing EMT in GBM-derived endothelial cells