Since STAT3 was downstream of the Wnt pathway, our data revealed that WP1066 reversed the proliferation promotion induced by PTGDS overexpression (Fig. 7E) and enhanced the proliferation inhibition (Fig. 7F) and apoptosis promotion (Fig. 7G) caused by AT56, indicating the involvement of STAT3 in the oncogenic role of PTGDS in DLBCL. Here, PTGDS is linked to diffuse large B-cell lymphoma.