Combining a cathepsin K inhibitor with human umbilical cord stem cell-derived extracellular vesicles at half doses achieved superior diabetic wound healing compared to full-dose single treatments in db/db diabetic mice. The mechanism centers on blocking ferroptosis, an iron-dependent cell death pathway that appears to impede wound repair in high-glucose environments. This dual approach enhanced collagen synthesis, cell migration, and blood vessel formation while requiring 50% fewer stem cell vesicles. The ferroptosis connection represents a significant mechanistic insight, as this cell death pathway has only recently been recognized as a therapeutic target in wound healing. For the millions with diabetic foot ulcers—a leading cause of amputation—this combination strategy could transform treatment by addressing two distinct pathways simultaneously. However, the research remains in early mouse models, and human trials will need to establish safety profiles for cathepsin K inhibition, which could theoretically affect bone remodeling. The ability to halve the dose of expensive stem cell-derived vesicles while improving outcomes could make regenerative therapies more clinically viable and cost-effective.