“…These include: (1) resistance to initial infection (Type I, incidence (INC)); resistance to fungal spread across the wheat head (Type II, severity (SEV)); resistance to kernel infection (Type III, Fusarium damaged kernels (FDK)); (2) tolerance to infection, and (3) accumulation of deoxynivalenol (DON) toxin (Type IV) [ 2 , 11 , 12 , 13 , 14 ]. Previous studies indicated that the genetic architectures of these different components are either only partially shared, or independent [ 12 , 15 , 16 , 17 ]. In addition to physiological (active) resistance mechanisms, developmental related traits like flowering time, plant height, and spike morphological traits also affect FHB resistance levels through disease escape (passive) mechanisms [ 12 , 14 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”