Under oncogenic stress, mitochondrial ROS overproduction can accelerate mutagenesis, which amplifies tumorigenic signaling and increases metastatic potential.63 Overexpression or activating-mutation of EGFR promotes tumor progression and metastasis.64 EGFR activity is implicated in DNA repair.65 Therefore, advanced ROS generation and increased cell survival via the combined effect of MCT-1 and EGFR may mis-repair oxidative DNA damage and promote growth of gene-mutated cells. Here, EGFR is linked to neoplasm.