Our research interests reside in intercellular neuronal communications critical for sensing the cues from the environment. This evolved us to study ephaptic inhibition between taste neurons in Drosophila, which our lab discovered and reported recently. In addition to the interaction between neighboring gustatory neurons we study, ephaptic coupling has been known to synchronize activities of adjacent neurons, contributing to generation of neural oscillations aka brain waves.  However, a lack of molecular mechanisms has hindered the neuroscience community from making progress in understanding of the implications and significance of ephaptic interaction. Our recent preprint paper at BioRxiv (https://www.biorxiv.org/content/10.1101/2023.08.04.551918v2) revealed that there is indeed a mechanism regulating ephaptic inhibition. Hyperpolarization of membrane potential has been suspected to underlie the inhibition of post-ephaptic neurons once pre-ephaptic partners are excited. We found that hyperpolarization-induced cation current mediated by 'Hyperpolarization-activated cyclic nucleotide gated channel' (HCN) allows post-ephaptic neurons to resist ephaptic hyperpolarization. Such reslience expressed in a partner neuron lateralizes the ephaptic interaction, enforcing sweetness dominance in Drosophilia taste interaction. This discovery highlights that ephaptic coupling is not a mere electrical interference or noise in the brain and is evolved to finely tune the activity of neighboring neurons. We are extending this finding to other sensory contexts, seeking out to unravel the meanings of intercellular communications in sensory contexts.