Over $100 billion is attributed to cereal cyst nematodes (_Heterodera_ spp.), with losses ranging from 20% to 90%, depending upon location and year [20; 22; 23]. _Meloidogyne graminicola_ of rice has resulted in yield losses of up to 80% in Southeast Asia [11; 24]. This nematode is also problematic in Latin America, Asia, Southeast Asia, and India where flooding is restricted in the interest of water conservation [4; 6]. In the PNW, the root lesion nematodes, _Pratylenchus neglectus_ and _P. thornei_, contribute up to 35% and 60% yield reductions in wheat, with yearly chronic losses of 5% ($51 million) [25; 26]. The cereal cyst nematodes _Heterodera avenue_ and _H. filipjevi_ ([PERSON], 1981) [PERSON], 1984 also are problems on PNW wheat and barley [5]. Solutions for nematode resistance likely will depend on the host-pathogen interaction, particularly on plant genotype and pathogen-specific aspects of the infection processes. Root-knot nematodes enter the root at the zone of elongation, and migrate intercellularly to the vascular cylinder, where they induce feeding sites composed of giant cells [9; 13]. Female nematodes deposit eggs onto the root surface in a gelatinous matrix. The nematodes also stimulate plant cell division resulting in an external organ, called the knot or gall. While little cellular damage occurs during the establishment of the feeding site, the nematode draws nutrients from the host, alters host root morphology, and generates progeny. In contrast, cereal cyst nematodes intracellularly migrate to the vascular cylinder, and induce the fusion of multiple host cells to form a multinucleate feeding organ called the syncytium [10; 13; 27]. The root lesion nematodes also intracellularly migrate through the root, causing significant host cell breakage. However, these nematodes feed from root cortical cells without disrupting the lignin and suberin layers of the vascular cylinder [13; 28]. popular in the 1980s and 1990s, and should be given consideration again in the light of CRISPR/Cas9 biotechnology that will eventually be refined for producing non-GM germplasm for the cereals [36; 37; 38; 39; 40]. Accordingly, Section 7 of the review includes new data on wheat root genes induced during infection by _Pratylenchus neglectus_ and _P. thornei_, the aim of which is to identify regulatory DNA segments with potential to turn on the expression of selected resistance genes when _Pratylenchus_ is present. Candidate defense genes for disease resistance in wheat, barley, or rice are sometimes found in non-cereals, necessitating a search for the cereal gene equivalent (orthologue). In this section, we also discuss attempts to identify the wheat orthologue of the _DORN1_ gene (also known as _P2 KI_) from Arabidopsis. The DORN1 (Does not Respond to Nucleotides1) protein is a plasma membrane-bound receptor that senses extracellular ATP released during cellular damage [41]. The gene was originally isolated using a genetic screen for an ATP-insensitive mutant [42]. When overexpressed in Arabidopsis (_Arabidopsis thaliana_ (L.) [PERSON]), tobacco (Nicotiana benthamiana Domin), and potato (_Solanum tuberosum_ [PERSON]), the Arabidopsis _DORN1_ gene conferred host resistance against the biotroph _Phyophthora brassicae_ [PERSON] [PERSON] 2002, the hemibiotrophs _Pseudomonas syringae_ [PERSON] and _Phytophthora infestans_ ([PERSON], and the necrotroph _Botrytis cinerea_ (Pers. :Fr) [43; 44; 45; 46]. Pathogen resistance resulted when the receptor-ATP complex triggered the release of reactive oxygen species (ROS) and activated additional defense pathways in the host [47; 48]. Root defense strategies and root interactions with the microbiome are reviewed in [PERSON] et al. [49].