<p>Renal cell carcinoma (RCC) is one of the primary drivers of cancer-related mortality worldwide. Despite advancements in cancer diagnosis and management, there is a lack of effective available treatment options for such patients. This is often attributed to late diagnosis, lack of biomarkers, and resistance against standard-of-care therapies. Thus, identifying novel targets in RCC is needed to improve disease outcomes. Cu is a trace element required for homeostasis, and its dysregulation is linked to cancer. Cuproptosis, a programmed cell death, occurs due to intracellular Cu overload, disrupting the TCA cycle, inducing oxidative stress, and impairing metabolism. In cancer, abnormal Cu levels drive Cu-dependent proliferation, termed cuproplasia. The role of cuproptosis and cuproplasia in RCC remains unclear; their comprehensive understanding will enable the discovery of novel targets for effective therapy. This review explores their molecular mechanisms, impact on RCC progression, and therapeutic potential.</p>