Mutations of genes encoding for proteins within the photorespiratory core cycle and associated processes are characterised by lethality under normal air but viability under elevated CO2 conditions. This feature has been described as ‘the photorespiratory phenotype' and assumed to be distinctly equal for all of these mutants. In recent years a broad collection of photorespiratory mutants has been isolated, which has allowed a comparative analysis. Distinct phenotypic features were observed when Arabidopsis thaliana mutants defective in photorespiratory enzymes were compared, and during shifts from elevated to ambient CO2 conditions. The exact reasons for the mutant-specific photorespiratory phenotypes are mostly unknown, but they indicate even more plasticity of photorespiratory metabolism. Moreover, a growing body of evidence was obtained that mutant features could be modulated by alterations of several factors, such as CO2:O2 ratios, photoperiod, light intensity, organic carbon supply and pathogens. Hence, systematic analyses of the responses to these factors appear to be crucial to unravel mechanisms how photorespiration adapts and interacts with the whole cellular metabolism. Here we review current knowledge regarding photorespiratory mutants and propose a new level of phenotypic sub-classification. Finally, we present further questions that should be addressed in the field of photorespiration.