The diversity of body colour patterns seen throughout nature arises from neural crest-derived chromatophores. Mammals and birds achieve a stunning variety of colour with a single chromatophore of the body, the melanocyte. Our cold-blooded relatives, fish, amphibians and reptiles typically have a larger palette to choose from, presenting most commonly with melanocytes, xanthophores and iridophores. Medaka are one of the minority of fish species which also form a forth white reflective cell type called the leucophore. The reflective nature of leucophore's purine-related, uric acid intracellular pigment elements had previously lead to the conclusion that leucophores were more closely related to silvery iridophores. Recently, however, both Nagao et al., and Kimura et al., make compelling cases for leucophores sharing a neural crest lineage with xanthophores instead. Medaka leucophore mutants have now begun to not reflect but shed some light on to the genetic switches required for both leucophore and xanthophore specification. Kimura et al., have identified the underlying causative genes for three leucophore mutants: leucophore-free/slc2a15b, lf-2/pax7a and white leucophore/slc2a11b (Kimura et al., 2014). All three mutants affect both leucophores and xanthophores initially highlighting the developmental relationship of the two chromatophores. Closer inspection reveals a more structured hierarchy where pax7a expression in neural crest cells precedes the appearance of all chromatophores and is required for the development of both leucophores and xanthophores in the trunk. Leucophore-free/slc2a15b mutants were shown to successfully establish leucophore and xanthophores precursor cells, but these cells failed to differentiate and pigment properly. White leucophore/slc2a11b mutants were also able to form both leucophore and xanthophore precursor cells, but these cells were defective in their ability to produce orange or yellow pigmentation. A phylogenetic tree based on the amino acid sequence of SLC2A class II transporters using ascidian and vertebrate orthologs also revealed a coupled presence of slc2a15b and slc2a11b in other animals presenting xanthophores. With a close developmental relationship between leucophores and xanthophores becoming clear, the ensuing crucial question remains what molecular switches are required to specify leucophores and xanthophores from their common precursor? As Nagao et al. (2014) nicely demonstrate that switch is governed by sox5. The many leucophores-3/sox5 mutants lack all visible xanthophores in both embryonic and larval stage medaka but have an expanded population of leucophores. Many leucophores-3/sox5 heterozygous fish also develop an increased population of leucophores and have a noticeable reduction in xanthophores. The semidominant nature of the phenotype points towards a sox5 dose-dependent relationship between the two chromatophores. Using reciprocating cell transplantation experiments between many leucophores-3/sox5 and wild-type embryos, it was revealed that the sox5 switch between leucophores and xanthophores works in a cell autonomous fashion. So, if sox5 is the switch, when is it used? Both leucophores and xanthophores depend on pax7a for the specification of their common precursors. Xanthophores then require the expression of sox5 whereas leucophores do not as lack of sox5 in many leucophores-3 leads to a complete shift to the leucophore lineage at the expense of xanthophores. With four chromatophore linages to be determined in medaka, what role does sox5 play in the lineage of xanthophores in fish species with only three chromatophore types? Does sox5 have other roles in the neural crest cells of animals completely lacking xanthophores? Armed with these new questions and a more detailed understanding of specific neural crest fate switches, it is only a matter of time.