YAP and TAZ are key downstream effectors of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration, and tumorigenesis. This review summarizes the current understanding of YAP and TAZ functions, how their regulation is disrupted in cancer, and their potential as therapeutic targets. The Hippo pathway was first identified in flies and is conserved in mammals, playing a critical role in cancer progression and organ development. The pathway consists of a kinase module and a transcriptional module. The kinase module includes MST1, MST2, LATS1, and LATS2, while the transcriptional module includes YAP and TAZ, which are closely related paralogues that mediate downstream effects of Hippo signaling. YAP and TAZ function as transcriptional co-activators that shuttle between the cytoplasm and nucleus, inducing expression of cell-proliferative and anti-apoptotic genes. When the Hippo kinase module is active, YAP and TAZ are phosphorylated and inactivated; when it is inactive, YAP and TAZ translocate to the nucleus and induce target gene expression. Recent studies have shown that YAP and TAZ are regulated by the microenvironment, extracellular signaling, and microRNA biogenesis. They are also involved in cancer progression and can act as oncogenes or tumor suppressors depending on the cellular context. YAP and TAZ are regulated by various pathways, including GPCRs, WNT, TGFβ, and BMP. Therapeutic targets for YAP and TAZ include small-molecule inhibitors such as verteporfin, which inhibits YAP-TEAD interactions, and peptides that mimic the function of VGLL4. Statins also regulate YAP and TAZ by inhibiting the mevalonate pathway. The Hippo pathway is involved in various cancers, and its dysregulation contributes to tumorigenesis. However, the pathway's role in cancer is complex, with YAP and TAZ functioning as both oncogenes and tumor suppressors depending on the tissue and cellular context. The study highlights the importance of understanding the regulation of YAP and TAZ in cancer and their potential as therapeutic targets.YAP and TAZ are key downstream effectors of the Hippo pathway, which regulates tissue homeostasis, organ size, regeneration, and tumorigenesis. This review summarizes the current understanding of YAP and TAZ functions, how their regulation is disrupted in cancer, and their potential as therapeutic targets. The Hippo pathway was first identified in flies and is conserved in mammals, playing a critical role in cancer progression and organ development. The pathway consists of a kinase module and a transcriptional module. The kinase module includes MST1, MST2, LATS1, and LATS2, while the transcriptional module includes YAP and TAZ, which are closely related paralogues that mediate downstream effects of Hippo signaling. YAP and TAZ function as transcriptional co-activators that shuttle between the cytoplasm and nucleus, inducing expression of cell-proliferative and anti-apoptotic genes. When the Hippo kinase module is active, YAP and TAZ are phosphorylated and inactivated; when it is inactive, YAP and TAZ translocate to the nucleus and induce target gene expression. Recent studies have shown that YAP and TAZ are regulated by the microenvironment, extracellular signaling, and microRNA biogenesis. They are also involved in cancer progression and can act as oncogenes or tumor suppressors depending on the cellular context. YAP and TAZ are regulated by various pathways, including GPCRs, WNT, TGFβ, and BMP. Therapeutic targets for YAP and TAZ include small-molecule inhibitors such as verteporfin, which inhibits YAP-TEAD interactions, and peptides that mimic the function of VGLL4. Statins also regulate YAP and TAZ by inhibiting the mevalonate pathway. The Hippo pathway is involved in various cancers, and its dysregulation contributes to tumorigenesis. However, the pathway's role in cancer is complex, with YAP and TAZ functioning as both oncogenes and tumor suppressors depending on the tissue and cellular context. The study highlights the importance of understanding the regulation of YAP and TAZ in cancer and their potential as therapeutic targets.