Research suggests that NDUFA4L2 plays a role in promoting glioblastoma progression and is associated with poor survival. However, the specific mechanisms and relationships between NDUFA4L2 and other factors, such as transcriptional regulation and mitochondrial fission, are still being explored. NDUFA4L2 may be effectively targeted by apatinib, although its interaction with other treatments, like sorafenib, is not entirely clear.