The spleen plays a key role in the pathogenesis of immune thrombocytopenia (ITP), as it is the main site of anti-platelet antibody production and T-cell-mediated autoimmune responses. 1 It is also involved in platelet pooling, sequestration and phagocytosis by red pulp macrophages. 1 These dysimmune processes are mediated by a complex interplay between immunologic triggers and immune mediators, including regulatory T cells (Treg), soluble cytokines, circulating microRNAs and surface immunoglobulin receptors on monocytes and histiocytes. 1,2 These immune functions justify the relevance of splenectomy as second-line therapy for ITP, with clinical response rates ranging from 50% to 70%. [3][4][5] Despite this, the recourse to splenectomy is progressively decreasing due to the risk of life-threatening complications, the long-term susceptibility to infections and the advent of alternative medical therapies. 5 To support therapeutic decisions, several studies have tried to identify clinical predictors of response to splenectomy. 6