FOXP4 maintains redox homeostasis in medulloblastoma via upregulation of SLC7A11 to suppress ferroptosis
This study demonstrates that FOXP4 is overexpressed in MB, especially in the high-risk Group 3 (G3) subtype, and correlates with poor patient prognosis, and provides a mechanistic rationale for targeting this pathway to enhance the efficacy of ferroptosis-inducing therapies, such as sorafenib, in high-risk MB.