TCIRG1 and osteopetrosis: This phenotype segregated with a monoallelic mutation in ATP6V1H. Since osteoporosis is the opposite of the osteopetrosis seen in Atp6i-deficient mice and expected for reduced V-ATPase activity, we studied the phenotype of zebrafish harboring a null mutation in atp6v1h. Indeed, this animal model displayed reduced bone mass, and we demonstrated that the bone defect was mediated by increased activity of mmp9 and mmp13.