We and other groups have demonstrated that through its transcription-dependent or -independent manners, NAC1 can activate Gadd45 cell survival pathway (Nakayama et al., 2007; Jinawath et al., 2009), promote autophagic response to mediate resistance to cisplatin (Zhang et al., 2012b), disable cellular senescence to enhance tumor initiation and development (Zhang et al., 2012a), regulate cancer cell cytokinesis to facilitate their incessant cellular divisions (Yap et al., 2012), and induce fatty acid metabolism (Ueda et al., 2010). This evidence concerns the gene NACC1 and cancer.