However, Vierra et al. proposed that patients with T2DM may develop two-pore domain K+ (K2P) channel TALK-1 disruption on δ cells, and may possibly be an explanation of the altered somatostatin secretion and secondary hyperglucagonemia, as TALK-1 channels are linked with both calcium intake by δ cells and somatostatin exocytosis [39] (Figure 2). The gene discussed is KCNK16; the disease is type 2 diabetes mellitus.