Mammalian cells have developed elaborate DNA damage response (DDR) and DNA repair systems in order when to protect and repair their DNA encountering toxic agents. In tumour cells, activation of these molecular events can make tumour cells resistant to chemotherapy or radiotherapy-induced DNA damage. Therefore, decoding how the DDR and DNA repair mechanisms are controlled is very important for understanding how cells become resistant to chemotherapy and to find ways to improve conventional cancer therapies. MCL-1 is a pro-survival protein that has multiple roles within the cell and has been shown to protect cells from death. It can interact with multiple important nuclear proteins involved in DDR response. Loss of MCL-1 increases genome instability after DNA damage. These studies indicate that MCL-1 may be an important component of the DDR machinery to regulate the repair of DNA lesions. Dr. Yemin Wang is investigating how MCL-1 regulates DDR and DNA repair. He is taking an intracellular approach to understand how MCL-1 is delivered into the nucleus after DNA damage and will also use this approach to investigate how MCL-1 regulates crucial events in DDR and DNA repair machinery. Dr. Wang will also examine whether the presence of MCL-1 in the nucleus affects how the cell responds to chemotherapy and whether the role of MCL-1 in DDR affects tumor development. The results of Dr. Wang’s work will provide us with a better understanding of MCL-1 in DDR and DNA repair processes, explain its essential function in vertebrate development, and help us to design improved therapeutic interventions for cancer treatment.