For radiation-responsive MSCs engineered with the SMAD-NIS system, their ability to enhance radiotherapy efficacy operates through two synergistic mechanisms: On one hand, TGF-β1-activated SMAD signaling strengthens the tumor-targeted migration of MSCs; on the other hand, the expression of the sodium-iodide symporter (NIS) drastically elevates the uptake of iodine-131 (131I) in tumors. The gene discussed is SLC5A5; the disease is neoplasm.