Persistence and re-emergence of fungal pathogens threatens the sweetpotato industry in North Carolina, which accounts for 60% of domestic supply and 80% of international exports. Ceratocystis fimbriata, a devastating soilborne pathogen and causal agent of black rot, imposes inevitable yield loss without aggressive cultural and chemical control management. European Union (EU) arbitrary changes in pesticide import tolerances for effective fungicides force rejections at port and loss of revenue for exporters and overseas customers. Deployment of multifaceted host resistance represents a desirable tool to decrease losses caused by C. fimbriata and other important pathogens. Our previous research pointed to a case of age-related resistance with contrasting root inner core phenotypes for younger developing roots as compared to older roots. We employed a contrast enhanced micro-CT analysis in an attempt to improve understanding of the mechanism controlling age related resistance. Infected root cells reacted to C. fimbriata infection by accumulating cells in the interphase that appears to prevent expansion of hyphae to the inner core of the sweetpotato storage root. In a broader impact approach, we aim to explore the sweetpotato innate immune system, which codes for intracellular immune receptors genes (NLRs). NLRs detect conserved effectors secreted by plant pathogens and trigger an immune response. Here, we apply a genome reduction approach (RenSeq) that facilitates cataloging NLR genes in sweetpotato cultivars. Our parallel approaches represent a game changing tool for breeders and producers to improve the resilience and disease management of sweetpotato under a changing climate.