A new study published in Cell Metabolism questioned the notion that type-1 diabetes (T1D) occurs due to a complete destruction of β cells, since small amounts of C-peptide are detectable in patients with long-standing T1D. This study entailed an analysis of protein and gene expression levels for proinsulin, insulin, C-peptide, and islet amyloid polypeptide within pancreatic tissues from T1D, autoantibody positive (Ab+), and control organs. It was observed that insulin and C-peptide levels ranged from low to undetectable in extracts from the T1D cohort. Whereas proinsulin and insulin (INS) mRNA were detected in a majority of T1D pancreata. Interestingly, heterogeneous nuclear RNA (hnRNA) for insulin and INS-IGF2, both originating from the INS promoter, were essentially undetectable in T1D pancreata, suggesting a silent INS promoter. Expression of PCSK1 – a convertase responsible for proinsulin processing, was reduced in T1D pancreata, supportive of persistent proinsulin. It was stated that the findings indicate the existence of β cells enriched for inefficient insulin/C-peptide production in T1D patients, potentially less susceptible to autoimmune destruction.