Cancer cells have unique energetic and biosynthetic demands that are fulfilled through the reprogramming of cell metabolism, thereby sustaining tumour progression. A frequently observed but poorly understood metabolic alteration occuring in cancer cells is the activation of de novo lipogenesis. Our work has focused on the oncogenic transcriptional co-activator YAP, a master regulator of organ size and tumourigenesis. Although YAP is known to be aberrantly activated in a number of human cancers, the mechanisms by which YAP promotes tumourigenesis are not well characterised. We find that YAP overexpression activates de novo lipogenesis in vitro. This occurs via YAP-induced transcriptional upregulation of serum- and glucocorticoid-regulated kinase 1 (SGK1), an effector of the oncogenic phosphoinositide 3-kinase (PI3K) pathway. Downstream of YAP, SGK1 promotes mTORC1 signalling, which in turn activates the master regulators of lipogenesis, sterol regulatory element-binding proteins 1/2 (SREBP1/2). Notably, we observe that inhibition of key enzymes involved in the de novo lipogenesis pathway blocks hyperproliferation associated with YAP-driven transformation. Our data reveal an important mechanism of crosstalk between two key oncogenic signaling pathways, highlighting a metabolic vulnerability that may be exploited in order to disrupt oncogenic YAP/PI3K activity.