While we have not definitively identified acini as the origin of Stc2 expression, Atf3, a downstream mediator of PERK signalling, accumulated only in acinar cells during CIP, suggesting that CIP treatment leads to a cell autonomous activation of Stc2. As observed in HEK293 and N2a neuroblastoma cells, the increased accumulation of Stc2 is consistent with activation of PERK signalling in response to injury [5]. The gene discussed is ATF3; the disease is hereditary sensory and autonomic neuropathy.