DNA replication is a highly coordinated process that ensures the accurate duplication of the genome. Various factors, both internal and external, can interfere with DNA replication. When this occurs, it is referred to as DNA replication stress. Cells employ a complex network of pathways to deal with replication problems. A key pathway that is activated in response to replication stress is mediated by the kinases ATR and CHK1. RecQL4 is a member of the RecQ helicase family of proteins and is involved both in DNA repair and DNA replication. In our study we aimed to unravel the elusive function of RecQL4 in DNA replication dynamics. Specifically, we studied RecQL4’s role in origin firing and fork progression under normal and replication stress conditions. To induce replication stress, we utilized inhibitors of the ATR and CHK1 kinases. Our findings revealed a crucial role of RecQL4 in regulating the timing and efficiency of origin firing under replication stress conditions. Specifically, RecQL4 was found to induce unscheduled origin firing and reduced fork rate in the presence of ATRi or CHK1i. Collectively, our study shed light on a novel function of RecQL4, underscoring its significance as a central orchestrator in maintaining genomic stability under replication stress conditions.