Protein folding occurring in the endoplasmic reticulum is extremely sensitive to environmental changes regarding, e.g., reactive oxygen species (which could be caused by, e.g., 177Lu-octreotate-induced radiolysis of water or downstream effects of irradiation-induced cellular damage), hypoxia, or inflammatory stimuli, and studies have shown that endoplasmic stress can induce apoptosis (mediated by, e.g., JNK signaling) and enhances the radiosensitivity of tumor cells by degradation of RAD51 and subsequent reduction of double-strand break repair [44, 45]. This evidence concerns the gene RAD51 and neoplasm.