Furthermore, the analysis of CCL2 expression pattern in insulin-containing islets (ICI) vs insulin-deficient islets (IDI) in T1D donors showed: i) the absence of CCL2 expression in IDI (Fig. 5C), ii) the increased expression of CCL2 in glucagon-producing cells within ICI respect to those present in IDI (p < 0.05), indicating that the presence of residual beta-cells triggers inflammation in other islet-endocrine cells also. The gene discussed is INS; the disease is type 1 diabetes mellitus.