The strong, positive correlation between aging and accumulation of somatic mutations has been well-documented in research. While most of these mutations remain inconsequential, if a cell does not repair this error before proliferation, it can become cancerous. Hematopoietic stem cells (HSCs) are a type of cell with the ability to duplicate and differentiate into all types of blood cells, including lymphocytes, monocytes, and erythrocytes. In rare circumstances, a mutation can arise in an HSC that creates a growth advantage, leading to the selective proliferation and overrepresentation of blood cells derived from these mutant “clones”. This process is known as clonal hematopoiesis, and mutations in genes involved in epigenetic regulation (TET2, DNMT3A, IDH2) are the major drivers of clonal hematopoiesis in humans. The medical term for the mutant expansion is clonal hematopoiesis of indeterminate potential (CHIP) where a mutated clone accounts for at least 4% of derived blood cells. Individuals with CHIP are at increased risk of developing hematologic malignancies, atherosclerosis, and myelodysplastic syndrome (MDS). HSCs mainly reside in the bone marrow, a dynamic heterogeneous environment characterized by cavities undergoing resorption and/or deposition activities. Cavities exhibiting both are known as M-type cavities, and these microdomains have been shown to support the proliferation of mutants specifically. Clinical data from TriNetX database on osteoporosis patients reveal that bisphosphonates, a class of drugs with anti-resorptive effect, reduce the risk for MDS. Using in vivo intravital imaging and peripheral blood analysis, we investigated the potential suppressive effect of zoledronic acid, the most commonly prescribed bisphosphonate, on inhibiting clonal expansion. While engraftment data from the peripheral blood analysis showed seemingly no suppressive effect, in vivo imaging depicted a clear decline in mutant clones, leading us to believe that secondary hematopoietic organs like the liver and spleen may play a previously unaccounted role in clonal hematopoiesis.