Several lines of evidence sustain that the LGV strains evolve to retain the CT135 activity in vitro: i) the passaging of the LGV-proctitis associated clinical isolate do not lead to the CT135 disruption (Fig 2); ii) CT135-null mutants did not arise even when the historical LGV prototype strain (L2/434/Bu) was continuously propagated in HeLa cells during over one year [15]; and iii) no CT135 polymorphisms were found within the population of any prototype strain from different LGV serovars (L1, L2 and L3) [46]. This evidence concerns the gene CIMAP1A and proctitis.