Notably, QKI was prioritized among candidate regulators based on three lines of evidence: firstly, QKI has been documented to possess tumor-suppressive functions with characteristic downregulation across multiple malignancies, including gastric carcinoma [15, 16]; secondly, a robust positive correlation between QKI and circUBE2G1 expression levels was identified in our clinical cohort; and most critically, computational prediction of high-affinity binding motifs within intron 5 (+722, +801) of UBE2G1 pre-mRNA was substantiated (Fig. S1A–C). This evidence concerns the gene UBE2G1 and neoplasm.