Developmental robustness is the ability to maintain organ size, shape and function, despite the presence of perturbation. Loss of this capacity may lead to altered body proportions after a local injury, affecting quality of life. The human body can recover from injuries in early development but this capacity declines postnatally, a decline that is not fully understood. We study this topic by analyzing how limbs recover a normal growth trajectory after a developmental insult in mouse, which is known as catch-up growth (CUG). We can induce the injury unilaterally (left limb) and in a transient manner. We successfully generated transient injury in the cartilage regions that form the scaffolds for future long bones, creating left-right limb asymmetry 3 days post-injury. This was done by transient expression of Diphtheria Toxin A (DTA) exclusively in the left limb chondrocytes, leaving the right limb as internal control. Our results showed that 6 days and 13 days post induced-injury, the left limb showed signs of recovery where the length of the left limbs was catching up with the contralateral ones. This behaviour was mainly associated with changes in cell size, not proliferation. We characterized the spatiotemporal expression of a readout of the mTORC1 pathway, known to be critical for cell size regulation in multiple organs, and found that it is upregulated in the left cartilage. We also found increased levels of cholesterol synthesis near the mTORC1-high cells, shortly after ectopic activation of mTORC1, suggesting that cholesterol metabolism is important to fuel the compensatory growth. Future experiments aim to identify the exact mechanism triggering mTORC1 activation, and the requirement/sufficiency of cholesterol to drive cartilage cell growth. In the long term, these experiments are expected to provide the groundwork for new treatments for growth disorders.