These above results are similar to the previous findings that deletion of a α-1, 3-Mannosyltransferase encoding gene ALG3, which is essential for N-glycosylation of secreted effector like Slp1, resulted in the arrest of secondary infection hyphae and a significant reduction in virulence, and thus made us presume that the constrained growth of MoPmt2 mutants might be ascribed to the failure of evading host innate immunity and thus attenuated virulence on host. This evidence concerns the gene ALG3 and infection.