This effect might be attributed to the reduced expressions of MHC class I molecules in the high SEC61G group, which aligns with the known role of SEC61G in stabilizing immune checkpoint ligands (ICLs), including PD-L1, PVR, and PD-L2, through glycosylation in EGFR-amplified glioblastoma multiforme (GBM) [36‒38]. The gene discussed is EGFR; the disease is glioblastoma.