Venomous animals have evolved diverse molecular mechanisms to incapacitate prey and defend against predators. The majority of venom components characterized to date disrupt the nervous, locomotor, and cardiovascular system or causes tissue damage and degradation. Our discovery that fish-hunting cone snails use weaponized insulins to induce hypoglycemic shock in prey provided an unusual example for the use of toxins that specifically target glucose homeostasis (1, 2). These insulins revealed new mechanisms of insulin receptor (IR) activation and inspired the design of novel drug leads for diabetes (3-6). Recently, we discovered that, in addition to insulins, the deadly fish hunter, Conus geographus, utilizes a weaponized somatostatin that potently blocks glucagon secretion thereby further exacerbating the hypoglycemic phenotype in prey (Yeung et al., unpublished). The native toxin is composed of a minimized cyclic somatostatin core motif linked to a heavily modified N-terminal tail that plays an important role for activating the somatostatin 2 receptor (SST2) in fish. The synergistic use of fast-acting insulins and SST2-selective somatostatins establishes glucose homeostasis as a target for prey capture and provides new opportunities for toxin-based diabetes drug design.