The translocation of EGFR into mitochondria has been shown to affect mitochondrial fission, energy production and metastasis in NSCLC.6 Moreover, the translocation of the related RTK, ErbB2, into mitochondria has been shown to affect the respiratory function of these organelles in breast cancer.7 In the present study, we demonstrate that overexpression of Tid1-S in cultured NSCLC cells enhances the mitochondrial accumulation of EGFR (Figure 2) and the migration and invasion abilities of these cells (Figure 4). The gene discussed is ERBB2; the disease is breast carcinoma.