A similar scenario was evidenced in bladder cancer, where TGF-β1 in CAF-conditioned medium led to phosphorylation of SMAD2 in cancer cells, resulting in the upregulation of ZEB2NAT. Such lncRNA demonstrated to be essential for TGFβ1-driven EMT, as ZEB2NAT depletion reversed CAF-induced acquisition of mesenchymal features and invasive phenotype, though the reduction of ZEB2 protein levels [50]. The gene discussed is TGFB1; the disease is urinary bladder cancer.