Concurrently, TTLL1 mediates glutamylation at YAP1’s E100 site—the GLS2–YAP1 interaction and YAP1 glutamylation act synergistically to promote the nuclear translocation of YAP1 and its transcriptional activation function, ultimately leading to PD-L1 upregulation and enabling pancreatic cancer cells to achieve immune evasion. This evidence concerns the gene CD274 and familial pancreatic carcinoma.