CRYBG3 is a gene encoding a protein with a crystallin beta-gamma domain that was initially characterized as a structural constituent of the eye lens involved in lens development 1. However, recent research reveals that CRYBG3 functions primarily as a long noncoding RNA (lncRNA) rather than through its protein product. LNC CRYBG3 acts as a multifunctional regulator with primarily tumor-suppressive properties in lung cancer contexts. Mechanistically, LNC CRYBG3 blocks cytokinesis and induces M-phase cell cycle arrest by directly binding G-actin and inhibiting its polymerization into contractile rings, consequently blocking the actin-MAL-SRF pathway required for cellular proliferation 2. Additionally, LNC CRYBG3 regulates cell division fidelity by directly binding Bub3 and disrupting the mitotic checkpoint complex, though this leads to aneuploidy when dysregulated 3. In response to ionizing radiation, LNC CRYBG3 is upregulated and suppresses cancer progression through mechanotransduction by dysregulating F-actin organization and inhibiting YAP/TAZ activity 4. Clinically, LNC CRYBG3 downregulation enhances radiosensitivity in NSCLC cells with wild-type p53 through reduced MDM2-mediated p53 degradation 5, suggesting therapeutic potential as a biomarker and treatment target for lung cancer.