The mechanisms underlying the connection between exposure to lead and cancer are not completely understood. Lead is thought to cause oxidative stress, impair DNA repair pathways, and contribute to inflammation, potentially increasing carcinogenesis. The involvement of the Symplekin in cancer biology induced by lead exposure is an emerging area of research. Symplekin is a crucial protein in RNA processing and polyadenylation and is essential for mRNA stability and translation. While the direct relationship between Symplekin and lead toxicity is not well documented, lead exposure has been linked to various cellular disruptions that can indirectly affect Symplekin function. By understanding the Symplekin's role in tight junctions, we can shed light on an innovative approach. Tight junctions assist in the maintenance and development of cell polarity by separating membrane proteins into separate domains on the basolateral and apical surfaces of epithelial cells. This polarity is necessary for cells to transport chemicals and respond efficiently to signals. Tight junctions facilitate the integration of signalling pathways that regulate cell behaviour and tissue homeostasis. Importantly, while some evidence suggests a possible link between lead exposure and cancer, more research is needed to establish conclusive connections. After recurrent exposure to lead in humans, the target organs are the haematopoietic system followed by other systems, but it is time to concentrate on the lead in the serum, which is minimal and has a high impact on systemic toxicity through tight junctions by disrupting Symplekin and associated protein homeostasis in the cells. Symplekin's involvement in mRNA processing and gene expression control places it within a larger network of cellular functions that, when interrupted, may contribute to cancer.