In line with observations of unchallenged Chd6-knockout mice, the mitochondrial deregulations again were also observed in AOM/DSS-treated Chd6-knockout mouse model (Fig. 5m), including reduced levels of TMEM65, PPOX, COX-IV, optic atrophy 1 (OPA1) and increased p-Drp1 level, suggesting that loss of impact of CHD6-TMEM65 axis on mitochondrial functions plays roles in alleviating tumor formation. The gene discussed is DNM1L; the disease is neoplasm.