The MHC mismatch itself promoted a pro-inflammatory microenvironment, amplifying T cell priming via cytokines such as IFN-γ and co-stimulatory signals (CD80/CD86), resulting in robust anti-tumor immunity, as evidenced by 70% of patients in NCT03697707 showing WT1-specific T cell responses and 45% achieving MRD-negative status, with minimal toxicities like GVHD. The gene discussed is CD86; the disease is neoplasm.