MYC and neoplasm: In addition, using a variety of experimental models, it has been later shown that upregulation of c‐MYC is sufficient to induce the formation of PDAC without additional genetic manipulation of any cell survival pathway (Lin et al, 2013), deletion of one c‐MYC allele decelerates tumor development in vivo (Walz et al, 2014), MYC targeted by an RNAi approach in vivo blocks PDAC development (Saborowski et al, 2014), and the subsequent increase in PGC‐1α is a key determinant for the OXPHOS dependency of cancer stem cells (Sancho et al, 2015).