It is possible, as above described, that if tumor PD-1 is in equilibrium with tumor PD-L1, the disruption of intratumoral PD1-PD-L1 induced by monoclonal antibodies that block PD-1 (nivolumab or pembrolizumab) or PD-L1 (atezolizumab, durvalumab and avelumab) can provoke tumor hyper-progression which has been reported in several studies (13) (Figure 1). The gene discussed is CD274; the disease is neoplasm.