Mitochondria are dynamic intracellular organelles that, in addition to being crucial for energy production, are key players during innate immune responses. Recently, the Youle lab found that in people with early-onset Parkinson’s disease, the loss of proteins responsible for eliminating damaged mitochondria can precipitate inflammation. Therefore, my research at the Youle lab will focus on the molecular mechanisms underlying the relationship between mitochondria and the innate immune response. Using molecular genetics, high-resolution microscopy, immunology, and cell biology techniques, I will explore how proteins involved in mitochondrial quality control regulate STING, a protein that detects cyclic dinucleotides produced either by invading bacteria or by the cell itself in response to free cytosolic DNA. I will assess whether inactivating these proteins in human cell lines promotes STING hyperactivation and triggers inflammation—work that could lead to new strategies for alleviating aberrant immune responses in people with Parkinson’s disease or other neurodegenerative disorders.