Figure 2: Mechanisms of physiological (a)-(b) and pathological (c)–(f) activation of FGFR3. (a) Monomeric inactive receptor; (b) Ligand-dependent dimerization and activation; (c) Ligand-independent dimerization and activation induced by mutation of the extracellular portion; (d) Ligand-independent activation due to mutations of the tyrosine-kinase domain; (e) Upregulation of signalling due to receptor overexpression; (f) Alteration of splicing favouring isoforms with broader ligand specificity.