We hypothesised that in melanoma resistant to PD-1 inhibitors, the use of mitochondria-targeting drugs to activate oxidative metabolism in melanoma and immune cells can not only increase the immune activity of CD8+ T cells (for example, the release of IFN-γ) but also inhibit tumour progression because of the altered energy metabolism balance by downregulating glycolysis. This evidence concerns the gene IFNG and neoplasm.