Despite significant advancements, immune checkpoint inhibitors (ICIs) targeting PD‐1, PD‐L1, and CTLA‐4 demonstrate limited efficacy in a subset of patients due to both inherent and acquired resistance.[33] Tumors frequently adapt by reshaping the tumor microenvironment (TME) to recruit immunosuppressive cells, including regulatory T cells (Tregs) and myeloid‐derived suppressor cells (MDSCs), which suppress antitumor immune responses. Here, CTLA4 is linked to neoplasm.