Of note while following the dynamics of soluble and tissue-based PD-L1 and IFNy at the time of major clinical responses, we observed that a sharp increase in soluble PD-L1 in plasma provided a better proxy at tumor progression to atezolizumab, indicating a mechanism of immune evasion that was only captured as biomarker in the liquid biopsy. The gene discussed is CD274; the disease is neoplasm.