Triptolide induces ferroptosis in various cancers by modulating key pathways at both gene and protein levels; it downregulates NRF2 in leukemia (K-562 and HL-60) cells, increasing ROS and lipid oxidation to sensitize cells to doxorubicin (DOX), inhibits GPX4 in glioblastoma (U-87 MG and U251-MG) cells through the NRF2/SLC7A11/GPX4 axis to promote lipid peroxide accumulation, and enhances ferroptosis in NSCLC (A549) cells by increasing ROS via the NF-κB pathway while simultaneously reducing drug resistance proteins such as P-gp and GPX4 [977, 996–998]. This evidence concerns the gene GPX4 and glioblastoma.