Histopathological analyses corroborated that JKE-1674–treated PPR-RFP prostate tumors, compared with vehicle-treated tumors, were largely well-differentiated and displayed higher expression of COX-2, a ferroptosis biomarker (28), along with a concomitant decrease in the frequency of mitotic cells positive for Ki67 staining (Figure 5D and Supplemental Figure 6E), suggesting that poorly differentiated and highly proliferative PPR-RFP tumor cells may be more vulnerable to ferroptosis induction. Here, MKI67 is linked to prostate neoplasm.