The role of the Golgi apparatus in carcinogenesis still remains unclear. A number of structural and functional cis-, medial-, and trans-Golgi proteins as well as a complexity of metabolic pathways which they mediate may indicate a central role of the Golgi apparatus in the development and progression of cancer. Pleiotropy of cellular function of the Golgi apparatus makes it a "metabolic heart" or a relay station of a cell, which combines multiple signaling pathways involved in carcinogenesis. Therefore, any damage to or structural abnormality of the Golgi apparatus, causing its fragmentation and/or biochemical dysregulation, results in an up- or downregulation of signaling pathways and may in turn promote tumor progression, as well as local nodal and distant metastases. Three alternative or parallel models of spatial and functional Golgi organization within tumor cells were proposed: (1) compacted Golgi structure, (2) normal Golgi structure with its increased activity, and (3) the Golgi fragmentation with ministacks formation. Regardless of the assumed model, the increased activity of oncogenesis initiators and promoters with inhibition of suppressor proteins results in an increased cell motility and migration, increased angiogenesis, significantly activated trafficking kinetics, proliferation, EMT induction, decreased susceptibility to apoptosis-inducing factors, and modulating immune response to tumor cell antigens. Eventually, this will lead to the increased metastatic potential of cancer cells and an increased risk of lymph node and distant metastases. This chapter provided an overview of the current state of knowledge of selected Golgi proteins, their role in cytophysiology as well as potential involvement in tumorigenesis.