Cancers with high levels of replication stress frequently acquire resistance to therapy and develop mechanisms to evade immune surveillance. Paradoxically, this replication stress also creates exploitable vulnerabilities. In this project, we aim to identify small‑molecule modulators of a recently uncovered regulatory mechanism within the Fanconi anaemia (FA) pathway, a central system for safeguarding replication fork stability and genome integrity. We have developed a novel, cell‑based nanoBRET assay optimised for high‑throughput screening in 384‑well format and have already identified and validated candidate modulators of this pathway. To advance these findings, we now seek to employ computational methods—including molecular docking, molecular dynamics simulations, and structural analysis—to elucidate the binding modes and mechanistic effects of these compounds on their FA pathway targets. Access to NAISS computational resources will be essential for enabling the large‑scale simulations and iterative modelling required to prioritise and refine these small‑molecule candidates.