In addition to osteoclast hyperactivation driving osteolytic lesions, recent studies have revealed a novel mechanism whereby exosomal miR-92a-1-5p from osteoblastic, osteoclastic, or mixed PCa subtypes promotes osteoclast differentiation while suppressing osteogenesis through the targeting of COL1A1, which encodes collagen type I alpha 1 chain, a major component of the bone ECM. The gene discussed is COL1A1; the disease is posterior cortical atrophy.