TRPV4 and dysplasia: If loss of TRPV4 function can lead to a decrease in the bone-absorbing osteoclasts and therefore a subtle increase in bone density, one might predict that GOF mutations could have the opposite effect of increasing osteoclast proliferation during development and resulting in hypoplasic skeletal defects underlying dysplasia, such as wafer-like vertebrae, brachydactyly, delayed carpal ossification, shortened trunk and limbs, facial hyperplasia, etc.