We report the case of an 8-month-old Caucasian girl referred to us for observation due to intense pallor, jaundice, lethargy and fever. Serological evaluations revealed severe anemia (Hb = 2.8g/dL) with a strongly positive direct antiglobulin test and high-titer warm IgG autoantibody. AIHA was diagnosed and steroid therapy with intravenous methylprednisolone at 2mg/kg/day was administered for 5 days (Figure 1 ). An adequate Hb increase was obtained and the child was discharged after 10 days with oral prednisone at 2mg/kg/day. During the subsequent months, several attempts were made to taper off the prednisone, but the patient had developed steroid dependence. Considering this dependence on high steroid doses, a therapeutic course with four doses of rituximab was performed (375mg/m 2 /dose) at weekly intervals ( Figure 1 ). Before rituximab infusion, serum immunoglobulin levels were normal and subpopulation lymphocyte counts were within the normal range. The treatment with rituximab was well tolerated and the patient received intravenous substitutive therapy with commercially available immunoglobulin preparations (400mg/kg, every 3 weeks for 6 months). One month after the end of the first course of rituximab, while still receiving low-dose steroids, the patient presented with a clinical relapse of AIHA, so prednisone was increased to 2mg/kg/day and two further rituximab infusions were performed ( Figure 1 ). After these infusions, B lymphocytes became undetectable and the count returned to normal values 8 months after treatment. The patient remained in clinical remission and free from immunosuppressive drugs for 7 months, before presenting with a further relapse. A more intensive treatment was performed ( Figure 1 ) with cyclophosphamide 10mg/kg/ day for 10 days and methylprednisolone 40mg/kg/day for 5 days, which was tapered over 20 days. Hb level increased and the patient was discharged 10 days later in good clinical condition, without any antifungal or antiviral prophylaxis.