Within the relatively rare clinical entity of kidney cancer, several pathological diagnoses can be distinguished, among which clear cell, papillary, and chromophobe carcinoma dominate in terms of frequency. The new classification of kidney cancer places special emphasis on distinguishing rare subtypes of kidney cancer based on molecular profiling. The molecular mechanism of the most common subtype of kidney cancer, clear cell, rests on the dysregulation of the VHL gene and its target protein pVHL, whose role is the production of HIF-1α. In hypoxic conditions, HIF1α is stabilized, its degradation is inhibited, which leads to its accumulation inside cells and its activation. Stabilized and accumulated HIF-1α leads to the activation of transcription of the VEGF gene, a key gene for angiogenesis, and GLUT1, a protein for glucose transport. The environment of a fast-growing tumor is in a state of relative hypoxia, therefore neoangiogenesis is a condition for supporting tumor growth, tumor adaptation and metabolic change to aerobic glycolysis. Clinical prognostic tools do not take into account either the histological type or the pathomorphological features of the tumor, and therapeutic options in the treatment of kidney cancer were until recently limited to oral therapy directed at vascular endothelial growth factor receptor tyrosine kinases or at bevacuzimab, a monoclonal antibody directed at the factor growth of the vascular endothelium, given that VEGF was the only recognized therapeutic target, and specific oncological treatment was reserved only for metastatic stages. New immunotherapy options are based on the expression of PD-1 receptor or PD-L1 expression within the tumor or tumor microenvironment. In this study, the expression of the HIF-1A gene and its target protein HIF-1α, as well as its downstream targets - VEGF and GLUT1, in the three most common types of kidney cancer was shown. A significantly higher nuclear expression of HIF-1α was observed in pRCC compared to ccRCC, while there was no significant difference in VEGF-A protein expression between the analyzed histological subtypes of RCC. GLUT1 is more expressed in ccRCC than in pRCC and chRCC, but there was no difference in GLUT1 expression depending on the grade of the RCC tumor, nor the size of the tumor. No statistical difference ih HIF1A expression between histological types using quantitative reverse transcription polymerase chain reaction was shown. The different results of the analyzed parameters prove the differences of oncogenesis among different subtypes of kidney cancer. Most of the studies published so far considered only the clear cell type of kidney cancer, this study included papillary and chromophobe kidney cancer. The different results of the analyzed parameters prove the differences of oncogenesis among different types of kidney cancer. A prospective study that would combine oncological outcomes in the results can additionally clarify the significance of the analyzed markers in clinical practice among different types of kidney cancer.