ADCs mediate their effects through two principal mechanisms: first, antibody-dependent cellular cytotoxicity (ADCC), mediated through Fcγ receptor engagement, recruits natural killer (NK) cells and macrophages to release tumor-associated antigens (TAAs) and damage-associated molecular patterns (DAMPs) [7, 8] and, second, the integration of ADCs and ICIs leverages ADC-induced antigen release and PD-L1 induction to overcome ICI resistance, creating a feedforward loop of immune activation [9, 10]. Here, CD274 is linked to neoplasm.