CD8A and neoplasm: While no specific drugs activating PGC1α are currently available, strategies to direct the metabolic reprogramming of T-cells such as enforcing expression of PGC1α [36] or 4-1BB co-stimulation of CD8+T-cells which engages PGC1α-mediated pathways via activation of p38-MAPK [37] result in enhanced mitochondrial capacity and have been shown to improve the anti-tumour effects of adoptive cell therapy.