Immune thrombocytopenia (ITP) is a heterogeneous disease characterized by low platelet counts due to an imbalance between effective and regulatory immune cells, leading to increased platelet clearance and impaired thrombopoiesis. The pathogenesis of ITP involves several mechanisms, including peripheral destruction of platelets opsonized by antiplatelet antibodies, impaired thrombopoiesis, and T-cell-mediated destruction of platelets. Despite advancements in understanding the underlying pathology, up to 75% of adult patients with ITP develop chronicity, posing a significant burden on their quality of life. Bleeding is a major risk associated with ITP, but the exact relationship between platelet count and bleeding symptoms remains unclear. Current management of ITP includes immune suppression (corticosteroids and intravenous immunoglobulins) and the use of thrombopoietin receptor agonists (TPO-RAs), rituximab, or spleen tyrosine kinase (Syk) inhibitors. Newer targeted therapies, such as Bruton's tyrosine kinase inhibitors, neonatal Fc receptors, strategies targeting B and plasma cells, strategies targeting T cells, complement inhibitors, and newer TPO-RAs, have shown promising results in improving patient outcomes. However, there is a lack of knowledge about predictive factors for treatment response, which could help optimize treatment algorithms for selected patients. The article reviews the pathogenesis of ITP, current treatment options, and emerging therapeutic targets. It highlights the importance of considering individual patient factors, such as bleeding phenotype, comorbidities, and patient preferences, in treatment decisions. The role of platelets in ITP and their immunological functions are also discussed. The article concludes by emphasizing the need for biomarkers to tailor individualized treatment options for patients with ITP.Immune thrombocytopenia (ITP) is a heterogeneous disease characterized by low platelet counts due to an imbalance between effective and regulatory immune cells, leading to increased platelet clearance and impaired thrombopoiesis. The pathogenesis of ITP involves several mechanisms, including peripheral destruction of platelets opsonized by antiplatelet antibodies, impaired thrombopoiesis, and T-cell-mediated destruction of platelets. Despite advancements in understanding the underlying pathology, up to 75% of adult patients with ITP develop chronicity, posing a significant burden on their quality of life. Bleeding is a major risk associated with ITP, but the exact relationship between platelet count and bleeding symptoms remains unclear. Current management of ITP includes immune suppression (corticosteroids and intravenous immunoglobulins) and the use of thrombopoietin receptor agonists (TPO-RAs), rituximab, or spleen tyrosine kinase (Syk) inhibitors. Newer targeted therapies, such as Bruton's tyrosine kinase inhibitors, neonatal Fc receptors, strategies targeting B and plasma cells, strategies targeting T cells, complement inhibitors, and newer TPO-RAs, have shown promising results in improving patient outcomes. However, there is a lack of knowledge about predictive factors for treatment response, which could help optimize treatment algorithms for selected patients. The article reviews the pathogenesis of ITP, current treatment options, and emerging therapeutic targets. It highlights the importance of considering individual patient factors, such as bleeding phenotype, comorbidities, and patient preferences, in treatment decisions. The role of platelets in ITP and their immunological functions are also discussed. The article concludes by emphasizing the need for biomarkers to tailor individualized treatment options for patients with ITP.