PTH signaling is essential for triggering matrix remodeling by osteocytes, a process that is critical in mediating calcium release and restoration in lactation and weaning, respectively.(20) Although this phenomenon has not been explored in CKD where high PTH is common, we hypothesized that osteocyte interactions with the bone matrix could contribute to the skeletal detriments in CKD, and that altered matrix composition and material properties can be detected in the perilacunar region when PTH is high but porosity is not evident. The gene discussed is PTH; the disease is chronic kidney disease.