The recent characterisation of MMP-9 expression and activity in mouse strains exhibiting variable susceptibility to sequelae of genital Chlamydia muridarum (MoPn) infection[5] supports this suggestion: C3H/HeN mice, which are particularly susceptible to fibrotic sequelae in this model[6], exhibited greater MMP-9 transcription and activity during infection. The gene discussed is MMP9; the disease is infection.