HAVCR2 and neoplasm: The mechanisms of acquired resistance to ICIs are multifactorial, complex, and dynamic, involving impairments in antigen presentation machinery, defects in IFN‐γ signaling, neoantigen depletion, tumor‐mediated immunosuppression or exclusion, upregulation of alternative T‐cell checkpoints (e.g., TIM3, LAG3, V‐domain immunoglobulin suppressor of T‐cell activation), and changes in the tumor microenvironment (TME) [23, 49, 50, 51].