Immune cells are majorly dysregulated in rheumatoid arthritis patients and are a major cause of pathogenesis and progression of this autoimmune condition. As mitochondria are master regulators of metabolism of all cells present in human body, it is of prime importance to study mitochondrial homeostasis in immune cells for identifying any dysfunction contributing to pathogenesis or progression of RA. The objective of our study is to understand the mitochondrial and mitochondrially driven alterations in immune cells of RA patients which may cause them to perform abnormal functions and may have an important contribution in progression of the disease.