Predators exploiting chemically defended prey are generally resistant to prey toxins. However, toxin resistance usually incurs a fitness cost and is therefore often lost when no longer needed. Bufonid toads are a frequently abundant food resource, but chemically defended by a group of cardiotonic steroids, bufadienolides. Bufophagous predators have evolved a specific and near-universal mechanism of resistance to these toxins, consisting of two amino acid substitutions in the Na+/K+-ATPase H1–H2 extracellular domain. The dynamics of loss or retention of this adaptation in secondarily non-bufophagous lineages remain inadequately understood. Here we explore thistopic by showing that the piscivorous banded water cobra Naja annulata retains the bufadienolide-resistant genotype of the otherwise toad-eating cobra clade. This confirms a trend for secondarily non-toad-eating snakes to retain bufadienolide resistance.