Enthesitis, or inflammation specific to sites in the body where tendon inserts into bone, can arise in isolated joints from overuse or in multiple joints as a complication of an autoimmune condition such as psoriatic arthritis or spondyloarthritis. However, the pathogenesis of enthesitis is not well understood, so treatment strategies are limited. A clinically relevant animal model of enthesitis would allow investigators to determine mechanisms driving the disease and evaluate novel therapies. Therefore, we developed a murine model of inducible enthesis-specific inflammation by constitutively activating the NF-κB pathway in Gli1+ cells. Gli1CreERT mice were crossed with IKKβ-overexpression mice and given tamoxifen injections 5 days postnatally to induce enthesitis. Sixteen weeks of IKKβ overexpression in enthesis cells led to impaired mechanical properties, subtle histologic changes, and changes to expression of extracellular matrix- and inflammation-related genes. Increased loading from treadmill overuse activity did not exacerbate this phenotype. Clinical significance:​ The new murine model may have utility for studying the pathogenesis of enthesitis and approaches to treat the condition.