Further work demonstrated that in muscular dystrophy (mdx) mice, the proliferation and survival of FAP cells depends on an intricate balance of TNF-α and TGF-β signaling, and that inhibition of TGF-β signaling through the use of the drug Nilotinib reduces FAP cell number and concurrent fibrosis in the mdx model [20]. The gene discussed is FAP; the disease is muscular dystrophy.