Overall, the modulation of the mitochondrial structure and the abnormal phenotypic appearance of the mitochondrial cristae point to physiological stress induced in RCC cells following the alterations we generated in the APOL1 gene, and suggest that abnormal mitochondrial metabolism levels are linked to APOL1 risk variants or lack of APOL1 expression. The gene discussed is APOL1; the disease is renal cell carcinoma.