Tunnelling nanotubes (TNTs) are long, transient actin-rich projections that mediate the intercellular transfer of various signals, organelles and pathogens. Although recent studies have highlighted some early steps in TNT formation, the molecular basis for their formation remains unclear. On page 4424, Chiara Zurzolo and colleagues investigate how TNTs are formed in neuronal CAD cells. Because neuronal cells are mostly immobile, the authors hypothesise that TNTs arise from dorsal filopodia, and analyse known inducers of this specific subset of filopodia. They show that overexpression of the unconventional actin-based motor protein MYO10 increases the number of TNTs, as well as the unidirectional transfer of vesicles between co-cultured cells. The authors next analyse deletion mutants of MYO10, and find that the full-length protein is necessary for the formation of functional TNTs. Moreover, both the motor and tail domains of MYO10 are required for TNT formation. The authors further examine the role of the tail domain, and identify the F2 lobe of the band 4.1, ezrin, radixin, moesin (FERM) domain within the MYO10 tail as being required for the formation and function of TNTs in the neuronal cells. Finally, the authors rule out activation of the Akt signalling pathway as having a role in the formation of TNTs under stress conditions, in contrast to what has been found in astrocytes. On the basis of these results, the authors propose that a specific subset of MYO10-dependent dorsal filopodia is the precursor of TNTs in neuronal cells.