One of the reasons for this could be that, at a higher dose PR8 was able to effectively antagonise the HDAC6, by either facilitating the degradation of its polypeptide or downregulating its enzymatic activity in WT mice to such an extent that it resembled the KO phenotype, hence skewing the comparison of the effect of infection between WT and KO mice. The gene discussed is HDAC6; the disease is infection.