Overexpression of GPC5 inhibits canonical wingless-type MMTV integration site family (Wnt)/β-catenin signaling to abrogate the interaction between Wnt3a and its cell surface receptor Frizzled8 by directly and competitively binding to the Wnt3a ligand at the surface of A549 lung adenocarcinoma cells [123,124]. The gene discussed is WNT3A; the disease is lung adenocarcinoma.