A single-cell multi-omics atlas of neuroendocrine carcinoma of the cervix identified DLL3 as a driver of immune evasion and validated DLL3-targeted therapy in patient-derived organoid models. The work links molecular heterogeneity to both tumour immune escape mechanisms and tractable therapeutic targeting. DLL3 has been explored in other neuroendocrine malignancies, and this study extends the rationale by tying target biology to immune interactions at single-cell resolution. For translational teams, organoid validation strengthens confidence that DLL3 targeting can affect tumour growth dynamics in patient-like systems. Further steps for clinical relevance include correlating DLL3 expression patterns with patient outcomes and determining whether immune evasion signals predict response to DLL3-directed agents.