Furthermore, we revealed that USP8 was a major downstream target protein of YAP/TEAD2-mediated transcriptional regulation and USP8-mediated de-ubiquitination is essentially responsible for the MHC-1 degradation and PD-L1 abundance of PCa, which is the leading molecular mechanism of ECM-derived PCa progression and immune evasion. This evidence concerns the gene TEAD2 and posterior cortical atrophy.