First, we clarify its two distinct mechanisms of action: (i) directly inhibiting laryngeal cancer cell proliferation and survival via the canonical vitamin D receptor (VDR) axis—triggering G0/G1 cell cycle arrest, inducing apoptosis, and reversing epithelial-mesenchymal transition (EMT); (ii) indirectly exerting anti-tumor effects by reprogramming the tumor immune microenvironment, including enhancing cytotoxicity of CD8+ T and natural killer (NK) cells, promoting dendritic cell maturation, and suppressing key inflammatory pathways such as the COX-2/PGE2 axis. The gene discussed is VDR; the disease is laryngeal carcinoma.