IFNG and neoplasm: Upon triple knockdown of exhaustion markers (PD-1, Tim-3, and Lag-3), CAR-T cells, which target the preS1 domain of HBsAg and exhibit the tumor-reactive marker CD39+ (preS1-CAR-T), potently inhibit tumor growth and increase IFNγ secretion in a patient-derived xenograft (PDX) mouse model [69].