Activation of the MAPK pathway via the TrkA agonist Gambogic Amide mitigated the protective effects of RBM25 silencing, in the HF + sh‐RBM25 group restored elevated levels of Caspase‐3 and Bax, suppressed Bcl‐2 expression, and significantly heightened the apoptosis rate, likely by reactivating downstream pro‐apoptotic signaling cascades such as mitochondrial dysfunction and PARP1 cleavage. The gene discussed is BAX; the disease is hydrops fetalis.