According to the results of network pharmacology, a preliminary prediction of the mechanism by which ZDF treats ITP may be as follows: ZDF inhibits the expression of Ras and prevents phosphorylation of its downstream effectors ERK, JNK, and p38, thus promoting platelet proliferation, immune regulation, and an anti-inflammatory effect. Here, MAPK1 is linked to autoimmune thrombocytopenic purpura.