Bladder cancer remains a prevalent and challenging malignancy. Myeloid-derived suppressor cells (MDSCs) have emerged as key contributors to the immunosuppressive tumor microenvironment, facilitating tumor progression, immune evasion, and resistance to therapies. This review explores the role of MDSC in bladder cancer, highlighting their involvement in immune regulation; tumor progression; and resistance to therapies such as bacillus Calmette–Guérin (BCG) therapy, chemotherapy, and immune checkpoint inhibitors (ICIs). We also discuss their potential as biomarkers and therapeutic targets, with current evidence suggesting that targeting MDSCs, either alone or in combination with existing treatments such as BCG and ICIs, may enhance anti-tumor immunity and improve clinical outcomes. However,, challenges remain, particularly regarding the identification and therapeutic modulation of MDSC subpopulations. Further research is warranted to fully elucidate their role in bladder cancer and to optimize MDSC-targeted therapies.

Immune checkpoint inhibitors used for metastatic clear cell renal cell carcinoma treatment show significant rates of complete response on metastatic sites. Feasibility of delayed surgery on primitive tumors remains questionable, especially regarding conservative procedures. We present here the first reported case of robotic-assisted partial nephrectomy (RAPN) and concomitant metastasectomy after long exposure to immunotherapy. We performed an imperative salvage RAPN and metastasectomy in a 79-year-old woman with history of right radical nephrectomy for oligometastatic clear cell renal cell carcinoma, previous open partial nephrectomy and ablative treatment on the remaining left kidney. In fact, after complete response on the metastatic sites, the patient experienced progression on the solitary kidney despite immunotherapy. This limited experience of RAPN and metastasectomy after long exposure to immunotherapy appears to be feasible safe and efficient both on the oncological and functional point of view.