In a recent study of a transgenic mouse model of pancreatic ductal adenocarcinoma with KRAS G12VD mutation and p53 heterozygous inactivation, Singh et al reported an analogous mechanism involving another NFAT family protein, NFATc1, which acts as a coactivator and transcriptional regulator of SOX2 (Singh et al., 2015). The gene discussed is KRAS; the disease is pancreatic ductal adenocarcinoma.