Iron Deficiency Anemia (IDA) remains a pervasive global health challenge, disproportionately affecting vulnerable populations such as women and children. This review explores the cutting-edge interplay between microRNAs (miRNAs) and proteins in erythropoiesis, highlighting novel therapeutic strategies for IDA. Emerging evidence underscores the pivotal role of miRNAs-such as miR-15a, miR-24, miR-150, and miR-223-in regulating erythropoiesis, with dysregulation linked to hematologic and systemic diseases. Proteins, acting as modulators of miRNA activity, present innovative pathways for intervention by influencing erythropoiesis at multiple stages, from stem cell proliferation to red blood cell maturation. Our synthesis highlights key molecular mechanisms: miR-15a suppresses erythropoiesis by inhibiting c-Myb, miR-24 impairs heme biosynthesis through ALK4 regulation, while miR-150 and miR-223 modulate critical hematopoietic pathways affecting cell differentiation and apoptosis. These miRNA-protein interactions suggest targeted therapies such as protein-based miRNA modulators could optimize erythropoiesis, advancing IDA management. Additionally, the review emphasizes the potential of leveraging protein-miRNA interactions for precision medicine, especially in resource-limited settings where anemia's burden is profound. By bridging current knowledge gaps, our proposed strategies offer personalized and scalable therapeutic solutions. This comprehensive perspective lays the groundwork for future interventions addressing one of the world's most widespread public health crises.