ARGRS+ tumor cells can communicate with T cell via many ligand-receptors (Supplementary Figure 8B), such as TIGIT-NECTIN2 [45] and LGALS9-CD44 [46], which were involved in suppressing tumor T cell infiltration, and promoted the cell state transition of immune cells towards a more immunosuppressive and exhaustive status, indicating the potential mechanism in mediating the dessert TME in the ARGRS-high group. Here, NECTIN2 is linked to neoplasm.