CD8A and neoplasm: In BAP1-mutated UM, researchers found that ITGB2-ICAM1 signaling was enhanced between terminally exhausted CD8+ T cells and GDF15hiATF3hiCDKN1Ahi tumor cells, and inhibiting either ICAM1 or ITGB2 could prevent liver metastasis in the BAP1-mutated patients (16).