To bridge this gap, our study: (i) Proposes disulfidptosis-driven subtypes for PCa risk stratification; (ii) Develops a Disulfidptosis Score (Dis score) integrating genomic and immune features; (iii) Validates CCNB2 as a therapeutic target through dual regulation of apoptosis and disulfidptosis - a mechanism previously unreported in PCa. This evidence concerns the gene CCNB2 and posterior cortical atrophy.