Results from these metabolic assays suggested that TFAM loss does alter HNC cell metabolism; however, the reprogramming seems to be the outcome of rewiring of intracellular metabolites but not external nutrient inputs and [2] Unlike the dogmatic role of ROS to trigger cell death, current findings surprisingly demonstrated that ROS level is elevated in mitochondrial defective TFAM-silenced HNC cells and increased ROS level likely plays a critical role in regulating tumour growth through the activation of pro-tumourgenic cues. Here, TFAM is linked to neoplasm.