During development, cell type-specific transcription factors determine a cell's final differentiation program, but this fate often has to be maintained for long after this point. An elegant way to maintain identity is autoregulation: transcription factors bind their own cis-regulatory sequences, ensuring their continued expression alongside that of their targets. However, a functional requirement for autoregulation in animal development had yet to be formally demonstrated, until now. Eduardo Leyva-Díaz and Oliver Hobert analyse autoregulation of the C. elegans transcription factor che-1 (a terminal selector for the ASE sensory neuron pair), using CRISPR/Cas9 to create che-1::gfp worms in which a CHE-1-binding site in the gene's own promoter is mutated. These mutants show defective salt chemotaxis (the main behavioural output of ASE neurons) and strongly reduced expression of CHE-1 target genes and che-1::gfp itself. These defects are observed in young animals and become progressively worse with age but, surprisingly, che-1::gfp expression is reduced even at the earliest stages of its expression, when it initially specifies ASE identity in the embryo. This reflects a requirement for autoregulation in the early amplification of che-1 expression: the authors find a substantial reduction in embryonic expression of a previously reported coding che-1 mutation (thanks again to a CRISPR/Cas9-generated GFP insertion). Thus, transcriptional autoregulation is functionally relevant in animal development, and autoregulation can occur right at the start of a terminal selector's expression, in initiation as well as in maintenance.