Agrin is overexpressed in hepatocellular carcinoma and promotes cellular proliferation [198]; further detailed analysis of this interaction has revealed that agrin acts as a bridge between both the integrin-linked kinase and Lrp4-MuSK pathways, transducing changes in extracellular matrix rigidity and ultimately resulting in the activation of the nuclear transcription factor YAP [199,200]; see commentary of Xiong and Mei [201]. The gene discussed is MUSK; the disease is hepatocellular carcinoma.