These analyses revealed that depletion of these genes resulted in increased phosphorylation of multiple signaling hubs, such as focal adhesion kinase (FAK) and its downstream targets p-38α and Hsp2714, Src-family kinases (SFKs) and signal transducer and activator of transcription 5a/b (STAT5a/b), 5'-adenosine monophosphate-activated protein kinase-α2 (AMPKα2) and its target CREB, which facilitates cancer cell adaptation to metabolic stress15, glycogen synthase kinase-3β (GSK3β), a key component of the Wnt pathway16, and platelet-derived growth factor receptor β (PDGFR-β) (Fig. 6c). Here, CREB1 is linked to cancer.