SLC7A11 and glioblastoma: Furthermore, inducing GBM ferroptosis is considered a research direction with therapeutic value.219 Sun et al.220 found that NF-κB activating protein (NKAP) binds with SLC7A11 m6A, recruits AS factors to proline-rich and glutamine-rich (SFPQ) recognition splice sites, performs transcription termination site (TTS) ASEs on SLC7A11 transcripts, inhibiting GBM ferroptosis.