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More than 30% of all human cancers contain activating mutations of the small G-protein RAS. As a result of this, RAS has been intensely studied and many efforts have been made to identify pathways that sustain RAS-driven transformation [1]. Recent studies have indicated that the transcription factor GATA2 is one of these partners in crime, but a mechanistic link between RAS and GATA2 had not been identified [2]. A paper in this issue of EMBO reports closes this gap showing that GATA2 can be activated by p38 in RAS-transformed cells [3].