In contrast, PI3K‐I and AMPK do not play a role in elevation of mTORC1 signaling in mutant‐COMP growth plate chondrocyte pathology (Fig. 2), whereas these molecules have been shown to play a role in neurodegenerative diseases,(55) obesity, inflammation, diabetes, and cancer.(56) These findings show that not all of the mechanisms regulating autophagy in other diseases are involved in the mutant‐COMP–induced autophagy block in growth plate chondrocytes. This evidence concerns the gene COMP and obesity due to melanocortin 4 receptor deficiency.