A preclinical study also revealed a better treatment response characterized by reduced tumor growth and increased median survival in a neuroendocrine mouse model treated with 177Lu-DOTA-JR11, an SSTR antagonist, compared to 177Lu-DOTA-octreotate, an SSTR agonist, by inducing two times more 53BP1 foci formation [132]. This evidence concerns the gene TP53BP1 and neoplasm.