This result, which was in agreement with the less prominent percentage of dystocia observed in the dKO (40%) females compared to the Mmp2−/− (54.5%) (Figure 1D), strongly suggests that the additional loss of Mmp9 against the background of Mmp2 loss (i.e., in dKO and Mmp2−/−, respectively) activates a compensatory mechanism that partially resolves the phenotype. The gene discussed is MMP9; the disease is dystocia.