Conversely, over-expression of PGC1α suppressed the reduction in cellular viability elicited by BRAF-inhibitors in BRAF V600E mutated melanoma model systems.Similar to the observations in melanoma, our group made the recent and related discovery that in glioblastoma targeting MET signaling, a receptor kinase that connects to the ERK signaling pathway, elicits an increase of oxidative metabolism through activation of fatty acid oxidation (FAO) [6]. Here, BRAF is linked to glioblastoma.