Flonicamid, a widely used insecticide, presents an intriguing question: does it function as an antifeedant by directly activating bitter-sensing gustatory receptor neurons (GRNs) in Drosophila melanogaster. Here, we found that electrophysiological recordings revealed that S-type labellar sensilla exhibited strong neuronal responses to flonicamid, while inhibition of bitter-sensing GRNs nullified this response. Genetic screening identified Gr28b, Gr93a, and Gr98b as essential gustatory receptors for flonicamid detection. Isoform-specific rescue experiments confirmed that Gr28b.a is responsible for restoring sensory responses in Gr28b mutants. Proboscis extension response assays demonstrated that wild-type flies avoided flonicamid, whereas Gr28b, Gr93a, and Gr98b mutants failed to. Functional rescue of these mutants restored the behavioral response, confirming the involvement of these receptors in mediating gustatory aversion. Our findings uncover a novel sensory mechanism for detecting flonicamid through specific gustatory receptors and highlight their potential as molecular targets for insect control strategies.