This is an erratum to the research article "WAPL functions as a rheostat of protocadherin isoform diversity that controls nerve conduction" published in Science, Volume 391, Number 6786, February 2026.[1] The article examines the regulation of protocadherin (Pcdh) gene expression in serotonergic neurons (5-HT) and olfactory sensory neurons (OSN) in mice.[1] WAPL, as an unloader of the cohesin complex, affects the diversity of Pcdh isoforms by regulating the translocation of cohesin to DNA.[1] A high level of WAPL in 5-HT neurons limits cohesin translocation, favoring the expression of the Pcdhαc2 isoform and leading to a pattern of axonal tiling.[1] Deletion of WAPL increases the probability of selecting promoters further away from the enhancer and increases the size of the loops at the Pcdh locus.[1] Loss of Pcdh diversity due to Rad21 deletion disrupts OSN axon convergence.[1] WAPL thus tunes the diversity of Pcdh isoforms according to neuron type and enables different modes of neural involvement.[1]