Interestingly, melanoma cells that were made resistant against the BRAFV600E-specific inhibitor and chemotherapy drug Vemurafenib possessed filamentous mitochondria.66 Conversely, knockdown of the fusion-promoting protein mitofusin 2 in melanoma cells induced a more fragmented mitochondrial phenotype and increased cell death upon Vemurafenib treatment.67 Therefore, our results might suggest that prevention or reversal of mitochondrial filamentation could be a strategy to overcome Vemurafenib resistance in BRAFV600E melanoma cells. This evidence concerns the gene MFN2 and melanoma.