This case report presents a 42-year-old female with heavy menstrual bleeding and syncope, initially diagnosed with AUB due to fibroids. The patient's hemoglobin (Hb) dropped from 11.8 g/dl to 7.3 g/dl within three days, despite multiple PRBC transfusions. Uterine artery embolization (UAE) was performed, but Hb levels continued to decline, prompting further investigation. Additional testing revealed normal iron studies, vitamin B12, and folic acid levels. The peripheral blood smear showed mild anisocytosis, and the ANA screen was negative. However, elevated lactate dehydrogenase (LDH) at 571 U/L, a positive DAT for IgG, and a reticulocyte count of 6.37 were observed. These findings were consistent with warm autoimmune hemolytic anemia (AIHA). Treatment with prednisone 60 mg/day was initiated, and subsequent transfusions used the least incompatible blood units. The patient was discharged with an improved Hb of 9.1 g/dl. Discussion: This case highlights the importance of considering AIHA in patients with persistent anemia, even when an apparent cause like AUB is present. The failure to achieve an adequate rise in Hb despite multiple transfusions was a key clue prompting further investigation. Elevated LDH and reticulocyte count, along with a positive DAT, are characteristic findings of warm AIHA. The overlapping etiology of anemia in this case presented a diagnostic challenge. AUB causes anemia through blood loss, while AIHA results from immune-mediated destruction of red blood cells (RBCs). The anemia from AUB may mask the hemolytic component of AIHA, making differentiation between the two causes difficult. Reticulocytosis, typically seen in AIHA, may be attributed to the body's response to blood loss rather than hemolysis. Elevated LDH and bilirubin levels, common in AIHA, might be less pronounced or overlooked in the context of recent blood loss. Characteristic AIHA findings like spherocytes or polychromasia may be less prominent when concurrent blood loss anemia is present. The smear may appear more consistent with iron deficiency anemia, which is common in chronic AUB. Misdiagnosis as simple blood loss anemia may result in inappropriate management, such as unnecessary iron supplementation or blood transfusions, which can exacerbate hemolysis in AIHA. In conclusion, diagnosing AIHA in the setting of anemia secondary to AUB requires a high index of suspicion, comprehensive laboratory evaluation, and careful clinical correlation. The possibility of masked AIHA should be considered in cases of persistent or worsening anemia despite adequate management of AUB. Early recognition and appropriate management of both conditions are crucial for optimal patient outcomes.