According to other reports, the blockade of JAK2 with ruxolitinib resulted in a positive therapeutic efficacy in psoriasis patients, and luteolin-7-glucoside and paeoniflorin compounds exerted their activity via JAK/STAT3 signaling in the IMQ-induced psoriasis-like murine model [40,41,42], suggesting prevention of psoriatic symptoms in IMQ-induced model by ADE treatment might be related to suppressive activity of ADE on activation of JAK/STAT signaling molecules. This evidence concerns the gene STAT3 and psoriasis.