In conclusion, the work described herein demonstrates that Talpha1 exhibits antiglioblastoma effects that are mediated through several channels including: (1) modulation of proapoptosis/survival genes leading to increased tumor cell sensitivity to oxidative stress or cytotoxic/chemotherapeutic agents; (2) promoting FasR-FasL-mediated immune cell killing cascades; (3) increasing target cell sensitivity to perforin-granzyme-mediated immune cell killing. Here, FASLG is linked to neoplasm.