How do organs achieve species-specific proportions despite remarkable differences in absolute size? The regulation of organ size and internal proportions during development is crucial for the proper functioning of our bodies, and yet it remains as one of the outstanding mysteries in developmental biology [1]. Limbs are well suited to study this topic, as they are dispensable and can be extensively manipulated without affecting embryonic viability. Moreover, by altering growth unilaterally, it is possible to maintain an internal control, which allows for intra-individual comparisons. We have developed new mouse models that enable induction of transient growth insults in the left but not the right hindlimb [2]. With this approach, we have recently shown that mosaic cell arrest in the left embryonic growth plate (the region that drives long-bone growth) does not lead to changes in bone length or width, due to the activation of local and systemic compensatory mechanisms [3]. We have now performed similar experiments with different insults: mosaic cell death in the whole limb mesenchyme, and overexpression of Connective Tissue Growth Factor (CTGF) in the growth plate. In both models, growth plate architecture is transiently disrupted and a severe limb asymmetry is generated, revealing that the efficacy of compensatory mechanisms depends on the insult type. Moreover, while internal bone proportions are preserved in the cell-death and cell-arrest models, the scaling mechanism of CTGF-overexpressing bones is disrupted. These models therefore provide a unique opportunity to study organ growth and scaling. I will discuss the extrinsic and intrinsic mechanisms potentially underlying the observed phenotypes.