Through in vitro and invivo experiments, we confirmed that knockdown of CD276 effectively improved thesensitivity of ccRCC cell models and animal models to sunitinib treatment.Mechanistically, such an effect of CD276 knockdown may be achieved throughinhibiting DNA damage repair processes and FAK-MAPK pathway activation toconsequently enhance the efficacy of sunitinib in killing ccRCC tumor cells. Here, CD276 is linked to neoplasm.