The 15 SNPs associated with FAW damage levels were in or closely linked to 7 genes (Table 1), two of which were not annotated. The other five included a cyclin with kinase activity to promote cell division (cyc3, Zm00001d036360); a protein disulfide isomerase member of the thioredoxin superfamily involved in starch synthesis (pdi1, Zm00001d049099); a late embryogenesis abundant (LEA) hydroxyproline-rich member of the glycoprotein family that is associated with the plasma membrane (Zm00001d008850); a protein kinase domain containing protein located in the nucleus (Zm00001d041826); and a cell wall-associated receptor kinase-like 8 (Zm00001d017264). Three of these genes (Zm00001d028785, Zm00001d041826, and Zm00001d049099) were previously found to increase expression following exposure to fungal pathogens (Hoopes et al., 2019 and Swart et al., 2017). Although none of the genes were part of annotated maize pathways, one (Zm00001d049099) is a thioredoxin, and the thioredoxin pathway was found to be associated with FAW damage levels (see below).