In vitro experiments showed that downregulation of MEG3 or overexpression of miR-125A-5P could facilitate Foxp3 transcription, inhibit RORγt expression, and lead to Treg/Th17 imbalance, which provided new ideas for elucidating the molecular mechanism of ITP. This evidence concerns the gene MEG3 and autoimmune thrombocytopenic purpura.