The authors present a compelling narrative on the role of cross-kingdom small RNAs (ck-sRNAs) in Botrytis cinerea virulence, but a deeper inspection reveals a significant overinterpretation of the evidence presented. The claim that ck-sRNAs contribute to the pathogen’s extraordinary host generalism by targeting diverse plant immune genes is not sufficiently substantiated by the data. Notably, the paper repeatedly emphasizes the variability of retrotransposon-derived sRNAs across populations and suggests a stochastic “shotgun” mechanism of host targeting. However, this hypothesis is presented without direct validation of sRNA functionality across the claimed 1600+ host species. The cited sRNA–host gene interactions are limited to a few model species (e.g., Arabidopsis, tomato), and the leap to generalize these findings across the entire host phylogeny is unsupported and premature. Without systematic in planta validation across a phylogenetically diverse host panel, the suggestion that sRNAs are evolving adaptively to modulate host immunity across plant lineages is speculative and potentially misleading.
Moreover, the genomic diversity analysis suffers from a critical methodological flaw. While the paper compiles an impressive number of historical genotyping studies (>10,000 strains), the underlying marker systems (boty / flipper presence, microsatellites) are poorly harmonized across datasets, and the metadata integration lacks statistical rigor. The authors donot account for sampling bias (e.g., overrepresentation of viticulture-associated strains), nor do they apply phylogenetically corrected models to dissect host versus geographic effects. The meta-analysis infers environmental and host-driven selection shaping diversity, yet provides no robust quantitative evidence beyond correlation. Most notably, their assertion that high genetic recombination contributes to host generalism are not reconciled with the absence of experimentally validated genotype-by-host phenotype data.