The fact that the reovirus signature was present in T2DM but not in MetS subjects is in line with the observation that inflammation in general contributes to the development of T2DM [10–12], and supports the finding that inhibition of inflammation (by blockade of IL-1 signaling) improves HbA1c levels in T2DM patients without changing insulin sensitivity, but not in non-diabetic subjects with MetS [53]. The gene discussed is IL1A; the disease is type 2 diabetes mellitus.