Remarkably, recruited by potent antigen presentation signal stimulation (Figure 5E), the HRD group had a large proportion of CD8+ Tex cells and cycling CD8+ Tex cell clonotypes with high expression of cytotoxic signatures (GZMK) as well as exhausted markers (PDCD1, CTLA4, LAG3 and TIGIT),[34, 35] which not only indicates their impaired antitumor effects but also, more importantly, highlights the tremendous potential of ICB therapy, specifically targeting CTLA4, PDCD1, LAG3, and TIGIT (Figure 5F,G), as promising therapeutic strategies for HRD tumors. This evidence concerns the gene CD8A and hypoparathyroidism-retardation-dysmorphism syndrome.