It is speculated that the wild-type anti-PD-L1 antibody blocks the PD-L1 induced by rosiglitazone and IFN-γ, but also bridges the Fc receptor on NK/T-like cells and PD-L1 on tumor organoids, promoting the attack of tumor organoids by NK/T-like cells [97]. The gene discussed is IFNG; the disease is neoplasm.