During development of the vertebrate face, right and left streams of neural crest cells migrate from the neural plate to the ventral side of the embryo to form the facial prominences. The migration, proliferation and patterning of these streams occurs independently of one another but needs to be similar enough to achieve facial symmetry. In the majority of cases, neural crest-derived facial prominences grow and fuse together successfully to form the upper lip. However, failure of fusion of the prominences leads to the most common human craniofacial abnormality: non-syndromic or isolated cleft lip with or without cleft palate. While fluctuating asymmetries in relatives of individuals with clefts have been detected, their cellular basis is still poorly understood. To address this shortcoming, Adrian Danescu, Joy Richman and colleagues now analyse cell movements in the mesenchymal cells of the chick frontonasal mass (a prominence that forms the facial midline and participates in lip fusion). Morphometric analysis reveals a process of convergence and extension that drives frontonasal morphogenesis, in a manner not driven by oriented cell division; rather, cytoskeletal regulation plays a key role, as a ROCK inhibitor (ROCKi) prevents extension in organ cultures. Prominence-wide mathematical analyses of cell movements reveals oscillating periods of order (cells moving similarly to their neighbours) and regional coordination of movement within but also between left and right sides; ROCKi reduces these temporal fluctuations and causes asymmetry. The authors also reveal oscillating patterns of divergence and convergence in cell movements over time. Thus, fluctuating cellular movements in the facial prominences may be a key source of developmental instability that contributes to clefting.