Studies using lung cancer epithelial cells reported a crosstalk between AMHR2 and BMPR2 causing enhanced SMAD2/3 phosphorylation upon loss of AMH or AMHR2,131 possibly via mixed-heteromeric receptor complexes driven by BMP ligands.93 Correspondingly, in these cancerous epithelial cells, siRNA depletion of AMH or AMHR2 drives EMT,131 suggesting inhibitory functions of AMH in EMT. The gene discussed is AMHR2; the disease is lung cancer.