The term inflammation originates from the Latin, inflammatio, meaning ‘setting on fire’, and in medicine it indicates the reaction of tissues to injuries induced by different causes. Classically, inflammation is a protective response, which involves many complex signals and aims to repair tissue and restore homeostasis [1]. However, dysregulated or prolonged inflammation states have been associated with many diseases, including type 2 diabetes [1]. Early connections between inflammation, obesity and type 2 diabetes were made in the 1990s, in both rodent models and humans [2, 3], and later substantiated by a large body of evidence (see [4–7] for recent reviews). Then, it was observed that pancreatic islet cells may also show signs of inflammation, including immune cell infiltration [8–10] and increased expression of cytokines and chemokines [11–13]. It has been shown that a proinflammatory milieu can lead to reduced beta cell function and survival [14–16]. Given the key role of beta cell impairment in the onset and progression of diabetes [17, 18], it is of utmost importance to shed light on the several features linking inflammation and islet cell dysfunction. This commentary on the ‘Islet inflammation in type 2 diabetes’ symposium at the EASD 2015 meeting focuses on a few general issues regarding the association between inflammation and the pancreatic islets in human type 2 diabetes. It is accompanied by articles that specifically address the mechanistic implications [19, 20] and therapeutic perspectives [21].