The article reviews the emerging roles of Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) in cancer. YAP and TAZ are key downstream effectors of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration, and tumorigenesis. The authors discuss the current understanding of the biological functions of YAP and TAZ, their regulation, and how their disruption can contribute to cancer progression. They highlight recent findings on the expanding roles of YAP and TAZ in cancer progression and describe potential therapeutic targets for these proteins. The regulation of YAP and TAZ is influenced by the microenvironment, extracellular signaling, and microRNA biogenesis. Hyperactivation of YAP and TAZ is common in various cancers, and their inactivation can reverse cancer features such as stem cell properties, epithelial-mesenchymal transition, and resistance to apoptosis. The oncogenic activation of YAP and TAZ can be mediated by mutations in genes like *KRAS*, *LKB1*, *GNAQ*, and *GNA11*, as well as viral oncoproteins. Additionally, YAP has been shown to function as a tumor suppressor in certain contexts, particularly by inhibiting WNT signaling and triggering apoptosis. The article concludes by discussing potential therapeutic strategies targeting YAP and TAZ, including small-molecule inhibitors like verteporfin and VGLL4-mimicking peptides, and the use of statins to inhibit the mevalonate pathway, which affects YAP and TAZ activity.The article reviews the emerging roles of Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) in cancer. YAP and TAZ are key downstream effectors of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration, and tumorigenesis. The authors discuss the current understanding of the biological functions of YAP and TAZ, their regulation, and how their disruption can contribute to cancer progression. They highlight recent findings on the expanding roles of YAP and TAZ in cancer progression and describe potential therapeutic targets for these proteins. The regulation of YAP and TAZ is influenced by the microenvironment, extracellular signaling, and microRNA biogenesis. Hyperactivation of YAP and TAZ is common in various cancers, and their inactivation can reverse cancer features such as stem cell properties, epithelial-mesenchymal transition, and resistance to apoptosis. The oncogenic activation of YAP and TAZ can be mediated by mutations in genes like *KRAS*, *LKB1*, *GNAQ*, and *GNA11*, as well as viral oncoproteins. Additionally, YAP has been shown to function as a tumor suppressor in certain contexts, particularly by inhibiting WNT signaling and triggering apoptosis. The article concludes by discussing potential therapeutic strategies targeting YAP and TAZ, including small-molecule inhibitors like verteporfin and VGLL4-mimicking peptides, and the use of statins to inhibit the mevalonate pathway, which affects YAP and TAZ activity.