The canonical TGFβ signalling pathway, which controls many developmental processes, involves ligand binding to a type 2 receptor kinase. This then phosphorylates a type 1 receptor, which activates a Smad-dependent pathway that controls gene transcription. Now, however, Julian Ng reports that TGFβ signals regulate axonal development in Drosophila mushroom body neurons through Smad-independent mechanisms (see p. 4025). Loss of the type 1 TGFβ receptor Baboon (Babo) causes axon overextension in these neurons, reports Ng, whereas Babo overexpression causes premature axon termination. Babo, he shows, acts independently of Smads, signalling instead through the actin cytoskeleton regulators Rho1 and Rac (Rho GTPases) and LIM kinase 1 (LIMK1). Furthermore, Babo acts upstream of the Drosophilatype 2 TGFβ receptors Wishful thinking and Punt, which regulate axon growth independently through LIMK1-dependent and -independent mechanisms. Finally, Ng shows that Babo also regulates the development of other Drosophila neurons independently of Smads, raising the possibility that non-canonical TGFβ signalling might also function in other developmental situations.