DNA replication is the core process that ensures faithful duplication of the genome in every cell of every organism. While the replication process is well-characterised in simple organisms, the regulation becomes increasingly complex in higher eukaryotes, such as humans. The human genome lacks consensus origin-defining sequences and is demarcated via a mix of epigenetic factors, including non-canonical DNA structures. Among these, G-quadruplexes (G4s) act as functional origin motifs via their co-occurrence with the origin G-rich repeated elements. Interestingly, the origin recognition complex (ORC) and RECQ4 possess high affinity to G4s. While ORC's role in origin licensing is well established, RECQ4's function remains unresolved. RECQ4, a multifunctional helicase, is involved in replication and DNA repair. However, its relevance in origin firing remains controversial as studies categorise it as essential or redundant. RECQ4 mutations are associated with three recessive disorders causing cancer predisposition. Contrastingly, the gene is overexpressed in various aggressive cancers, including osteosarcomas. These studies belie the biological and clinical significance of RECQ4. Given that unchecked replication potential is a hallmark of cancer, RECQ4's function in replication, when altered, may induce carcinogenesis. Interestingly, recent studies also suggest that RECQ4's role in replication may be context-dependent and associated with its phosphorylation status. Further, studies from the host lab have demonstrated that RECQ4 interacts with G4 with high affinity, leading to biomolecular condensation in vitro. This project aims to link these findings and reconcile the controversies regarding RECQ4's function. We propose that RECQ4-G4 condensates likely act as spatial organisers of replication origins, regulated by protein-protein/protein-nucleic acid interactions and post-translational modifications.