Barley spot form net blotch (SFNB) caused by Pyrenophora teres f. maculata (Ptm) and Fusarium head blight (FHB) caused by Fusarium graminearum are devastating diseases of barley requiring advanced molecular breeding tools for disease management. I used genetic mapping and host-induced gene silencing (HIGS) to identify novel host genes and target existing pathogen genes to improve disease resistance in barley. Barley resistance to SFNB is often isolate specific and the Idaho isolate 13MI8.3 has a unique virulence profile. Two recombinant inbred mapping populations were utilized to characterize and map 13IM8.3 resistance. Quantitative trait loci (QTL) analysis revealed 10 significant resistance/susceptibility loci, including a previously unidentified QTL on chromosome 5H and the Rpt4 locus on chromosome 7H containing a dominant susceptibility gene (Sptm1) for broad-spectrum susceptibility to SFNB. Fine mapping of the Rpt4 locus in a F2:3 population derived from the cross Tradition (S) × PI 67381 (R) anchored the Sptm1 gene to a 400 kb region on chromosome 7H, and a putative cold-responsive protein kinase gene (HORVU.MOREX.r3.7HG0735560) was identified as a strong candidate and potential target for gene editing. As for the FHB management, HIGS was employed to silence the fungal gene FgGCN5 using the barley line Golden Promise. The FgGCN5 gene encodes a histone acetyltransferase which is essential for the F. graminearum growth. Despite demonstrated production of FgGCN5 small-interfering RNAs in the transgenic barley; the disease severity, DON accumulation, and fungal biomass showed no difference from wild-type. This research allows for more in depth analysis for the use of HIGS against FHB. Use of genetic maps, QTL, molecular markers, and transgenic technology in this research will benefit barley breeders, growers, and the industry in developing resistance to these important diseases.