A study published in *Nature Medicine* reveals that matrix-embedded cells, specifically hypertrophic chondrocytes and osteocytes, are essential sources of RANKL, a cytokine critical for osteoclast formation and bone remodeling. Traditionally, it was believed that osteoblasts or their precursors supplied RANKL, but this research challenges that notion. Using conditional mouse models and Cre-deleter strains, the study demonstrates that RANKL produced by hypertrophic chondrocytes is essential for resorbing calcified cartilage during bone growth, while RANKL from osteocytes is crucial for bone remodeling. Osteocyte-derived RANKL is also responsible for bone loss associated with unloading. The findings suggest that the rate-limiting step in matrix resorption is controlled by cells embedded within the matrix itself. The study also shows that RANKL produced by osteoblasts or their progenitors does not contribute to bone remodeling. These results highlight the critical role of matrix-embedded cells in regulating osteoclast formation and bone remodeling, providing a mechanistic explanation for the targeted nature of bone remodeling processes. The study underscores the importance of osteocytes in sensing mechanical forces and responding to changes in the bone matrix, which is essential for maintaining bone homeostasis. The research also indicates that RANKL produced by hypertrophic chondrocytes is necessary for the resorption of the primary spongiosa during bone development. The study's findings challenge the traditional view of osteoblasts as the primary source of RANKL and emphasize the role of matrix-embedded cells in bone remodeling. The results have implications for understanding and treating bone disorders associated with abnormal remodeling, such as osteoporosis and osteolysis.A study published in *Nature Medicine* reveals that matrix-embedded cells, specifically hypertrophic chondrocytes and osteocytes, are essential sources of RANKL, a cytokine critical for osteoclast formation and bone remodeling. Traditionally, it was believed that osteoblasts or their precursors supplied RANKL, but this research challenges that notion. Using conditional mouse models and Cre-deleter strains, the study demonstrates that RANKL produced by hypertrophic chondrocytes is essential for resorbing calcified cartilage during bone growth, while RANKL from osteocytes is crucial for bone remodeling. Osteocyte-derived RANKL is also responsible for bone loss associated with unloading. The findings suggest that the rate-limiting step in matrix resorption is controlled by cells embedded within the matrix itself. The study also shows that RANKL produced by osteoblasts or their progenitors does not contribute to bone remodeling. These results highlight the critical role of matrix-embedded cells in regulating osteoclast formation and bone remodeling, providing a mechanistic explanation for the targeted nature of bone remodeling processes. The study underscores the importance of osteocytes in sensing mechanical forces and responding to changes in the bone matrix, which is essential for maintaining bone homeostasis. The research also indicates that RANKL produced by hypertrophic chondrocytes is necessary for the resorption of the primary spongiosa during bone development. The study's findings challenge the traditional view of osteoblasts as the primary source of RANKL and emphasize the role of matrix-embedded cells in bone remodeling. The results have implications for understanding and treating bone disorders associated with abnormal remodeling, such as osteoporosis and osteolysis.