The robust efficacy of this regimen is attributed to a synergistic mechanism: bevacizumab’s inhibition of VEGF not only limits tumor angiogenesis but also re-models the immunosuppressive tumor microenvironment, thereby enhancing T-cell infiltration and the anti-tumor activity of atezolizumab’s PD-L1 blockade [6,7,8]. This evidence concerns the gene CD274 and neoplasm.