Since NpB-UV9 is as pathogenic as Np-B, except for the size of the cankers induced by the infection that are 1.6-fold bigger for NpB-UV9 than for Np-B (Figure 2), these results suggest that the ability of NpB-UV9 to produce high levels of (R)-mellein is associated with the induction of larger external cankers. Here, NPB is linked to infection.