The American chestnut is critically endangered due to the introduction of the chestnut blight fungus (Cryphonectria parasitica (Murr.) Barr) from Asia. The disease was first discovered in the Bronx Zoological Park (New York, USA). The pathogen infects the trees through the stem through wounds or cracks in the bark.  Symptoms of the disease include the formation of crankers, mycelial growth in the inner bark and appearance of orange fruiting bodies, which disperse spores by the wind. The fungus can also persist as a saprophyte.  In addition to chestnut blight, the wild-type trees are also susceptible to root rot caused by Phytophthora cinnamomi.

The fungus invades the tree by secreting oxalic acid into kill living tissue. Oxalic acid acidifies host tissues to toxic levels, chelates calcium ions from cell wall pectin, suppresses reactive oxygen burst and promotes programmed cell death. The pathogen does not exclusively rely on oxalic acid to infect the tree. Thus, in  trees containing a transgene or endogenous OxO gene, the fungal damage is lessened and the lifecycle is more saprophytic (not necrotrophic).

The original petition submitted to APHIS in 2020 identified Darling 58 as the event under consideration. Subsequent analyses determined that essentially all offspring from the initial crosses were derived from Darling 54 instead. The petition was therefore revised in August 2024 to identify Darling 54 as the event represented by most of the offspring data in the original submission. Darling 58 remains a distinct transformation event with the same genetic background and transgene construct as Darling 54 but a different genomic insertion site.