Although the exact mechanisms by which TGFβ and NFATc1 elicit opposing effects on pro-tumorigenic transcription programs remain to be elucidated, our findings underscore the strong context-dependency of TGFβ- and NFATc1-controlled transcription programs and emphasize that pharmacological targeting of these programs in PDAC requires careful consideration of the molecular makeup of a given tumor cell. This evidence concerns the gene TGFB1 and neoplasm.