Tendon injuries heal by forming a disorganized and mechanically inferior scar, whose properties improve over time but do not return to normal levels. Studies have shown that the exogenous application of cytokines, which are signaling molecules that play an important role in the wound healing process, to injured tendons can improve these inferior properties. Although such experiments are straightforward to perform, these studies often report conflicting results due to the many factors associated with exogenous application, such as the correct dosage, timing, and method of delivery. Therefore, in this study, a transgenic mouse injury model was developed and utilized to investigate the role of interleukin-4 (IL-4) and interleukin-6 (IL-6) in tendon healing through their absence. Overall, it was hypothesized that the lack of IL-4 or IL-6 would result in opposing effects on mechanical and organizational properties, with the lack of IL-6 resulting in superior properties. Overall, the results of the analyses for the uninjured tendons were as hypothesized. However, the results of the analyses for the injured tendons were not magnified with the addition of an injury but were instead found to be opposite. This study shows that a certain level of inflammation is necessary for tendon healing to occur, and it also demonstrates that a distinct and reproducible tendon injury can be created and tested in mice and supports the future use of this animal model to investigate the role of cytokines in tendon healing.