This hypothesis is supported by our preliminary RNAi screen data where the gene unc-31, the C. elegans equivalent of CAPS (a key component in Ca2+-dependent exocytosis of DCVs and regulation of cargo release) [36,37], emerged as a significant suppressor of ribosome deficiency-induced larval quiescence (Fig 7A). The gene discussed is CADPS; the disease is hyperinsulinemic hypoglycemia, familial, 4.