T cell immunoglobulin and mucin domain‐3 (TIM‐3), originally identified as a T helper (Th) 1‐specific type I membrane protein, plays a vital role in Th1 immunity and tolerance induction through interaction with its ligand, galectin‐9. The binding of TIM‐3 by galectin‐9 serves to downregulate Th1 responses. Moreover, the regulatory function of TIM‐3 has been extended to other cells, such as Th17 cells, CD4⁺CD25⁺ regulatory T cells (Tregs), CD8⁺ T cells and certain innate immune cells. Previous studies have acknowledged that the TIM‐3 pathway is involved in the pathogenesis of several human autoimmune diseases, such as systemic lupus erythematous, rheumatoid arthritis and aplastic anaemia. Moreover, genetic data suggest a role for TIM‐3 in human autoimmune diseases. However, in immune thrombocytopenia (ITP), a common Th1‐ and possibly Th17‐biased autoimmune disorder, the role of TIM‐3 has not been explored. Recently, our data have demonstrated that TIM‐3 expression is reduced in ITP patients, and we have found a potential link between ITP and the TIM‐3 pathway. In this article, we discuss and speculate on the role of the TIM‐3 pathway in ITP.