In a mouse lung cancer model, IFN-γ was observed to cause phase separation of Yes-associated protein (YAP) to form condensation and translocate to the nucleus to form a potent transcription center, promoting the expression of multiple genes, including CD155 (ligand for TIGIT), leading to CTLs function inhibition and anti-PD-1 resistance (90). The gene discussed is PDCD1; the disease is lung cancer.