Pigmentation has several functions ranging from protection from UV irradiation, to mating display, warning, and camouflage. Of all organisms fish exhibit some of the most remarkable variations in pigmentation and as a model organism the zebrafish, and more recently medaka, have played a significant role in determining which genes are implicated in the genesis of different kinds of pigment cells. It is now well established, not least through papers published in this journal, that fish can get a suntan, change pigment aggregation and dispersal in response to different wavelengths of light, and can also adapt pigmentation patterns to match their background. In the paper from Hatamoto and Shinyoji, a new aspect of the regulation of zebrafish pigmentation patterns is revealed. The ability of zebrafish to alter their pigmentation pattern to match their background appears to be a cognitive process involving the processing of visual information that is then relayed to the melanophores to adapt their pigment aggregation/dispersal. The consequence is that adaptation to differing background patterns can be learned and the fish trained to respond more rapidly to a changing environment. The exciting prospect is that the power of zebrafish genetics may be turned to dissecting the pathways involved implementing the pigmentation changes in response to the environment. The response of a whole organism like a zebrafish to the environment is readily observable. But at the cellular level the changing environment encountered by cells during development drives the generation of stem cells in their niche, as well as the migration of melanoblasts from the neural crest. In melanoma, it is increasingly recognized that while mutation of genes that promote proliferation or bypass senescence is a critical early step, the tumor microenvironment plays a major role in disease progression. For example, the access of cells to nutrients and oxygen may vary substantially within different regions of a tumor, as will contact with fibroblasts, macrophages and other non-tumor types. Understanding how the microenvironment influences tumor progression is therefore a key issue that lies at the heart of melanoma research. In this issue, two reviews focus on different aspects of how the microenvironment impacts on melanoma. In the first, Postovit et al. examine the role of Nodal and the microenvironment in melanoma plasticity. Particularly important is the concept that a melanoma does not contain a homogenous population of cells, but is rather made up of different subpopulations with phenotypes ranging from stem cells to differentiated cells. The review highlights the fact that each subpopulation is dynamic and switchable. In other words, specific cues in the microenvironment can drive cells from one subpopulation to another via epigenetic mechanisms rather than the acquisition of genetic lesions. The second review from Hersey and Zhang, take a different angle on the role of the microenvironment. Here the emphasis is on stress to the endoplasmic reticulum driven by the kinds of conditions encountered within a tumor such as anoxia or hypoglycemia. The output from ER stress may range form senescence to autophagy or apoptosis and for melanoma cells to survive they are likely to exploit adaptive mechanisms that enable to bypass the detrimental consequences of ER stress.