In an attempt to identify the mechanism for K-RAS independency in PDAC, Kapoor and colleagues [50] discovered that, upon K-RAS suppression, about half of the tumors relapsed thanks to activation of a transcriptional program controlled by the cooperation of the Yes-Associated Protein 1/TEA Domain Transcription Factor 2 (YAP1/TEAD2) transcription factors complex to promote cell cycle, DNA replication, and tumor maintenance in the absence of oncogenic K-RAS. The gene discussed is TEAD2; the disease is neoplasm.