Based on the premise that Em possesses anti‐post‐stroke depressive effects, we utilized network pharmacology and molecular docking techniques to predict core targets, including NFKB1, MAPK3, AKT1, BDNF, CASP3, JUN, TNF, and IL6, with BDNF being identified as the target with the highest binding affinity. Here, AKT1 is linked to stroke disorder.