Recent studies have shown that FLNC interacts with Dishevelled-2 (Dvl2) to activate the Wnt/β-catenin signaling pathway and regulate skeletal muscle development, whereas FLNC deficiency induces autophagy or mitosis and contributes to muscle atrophy (26), processes which have recently been implicated as key factors in the progression of BPH and the development of LUTS (18, 27). Here, DVL2 is linked to benign prostatic hyperplasia.