Kv11.1 encodes a voltage-gated potassium channel subunit belonging to the group of electrically silent Kv subunits, i.e., subunits that do not form functional homotetrameric channels. Kv11.1 has been shown to form heterotetrameric channels with voltage-gated potassium channel Kv2.1, which plays an important modulatory role in the glucose-dependent insulin secretion as it is the major contributor to the repolarization of the pancreatic (-cell. In the present study, we generated transgenic mice in which Kv11.1 is overexpressed to explore the physiological role of Kv11.1. Overexpression of Kv11.1 lead to an increase in insulin secretion which was glucose-independent, suggesting a role of silent channels in the regulation of the resting membrane potential and repolarization in the b-cells of the pancreas. We did not detect additional abnormalities in activity and exploratory behavior, neuromotor performance and cognitive performance. The results are compatible with the hypothesis that overexpression of Kv11.1 displaces the normal silent subunit interacting with Kv2.1 in b-cells.