Scientists have identified ZIP10, a zinc transport protein encoded by the SLC39A10 gene, as a critical regulator maintaining zinc levels in red blood cell precursors during periods of dietary zinc restriction. Through nutrigenomic analysis combining functional genomics with human genetic data, researchers demonstrated that ZIP10 responds dynamically to zinc availability and plays an essential role in erythropoiesis—the process of red blood cell formation. This discovery bridges a significant gap in understanding how micronutrient deficiencies translate into hematological disorders at the molecular level. The finding has particular relevance for global health, given that zinc deficiency affects nearly two billion people worldwide and frequently co-occurs with iron-deficiency anemia in vulnerable populations including pregnant women and children in developing regions. The identification of genetic variants in SLC39A10 associated with anemia risk suggests that individual differences in zinc transport efficiency may explain why some people develop anemia more readily than others under similar nutritional conditions. This nutrigenomic approach—examining how genes respond to nutritional inputs—represents an emerging paradigm for understanding personalized nutrition needs and could eventually inform targeted interventions for preventing nutritional anemias based on individual genetic profiles.