Since T2D is characterized by both a loss of insulin sensitivity of target tissues (fat, skeletal muscle, liver) and ultimately, impaired insulin secretion from the pancreatic β-cell1–3, these data raised the question: could impaired SWELL1-mediated signaling contribute to T2D pathogenesis, and if so, could this be corrected pharmacologically to improve systemic glycemia? Here, INS is linked to type 2 diabetes mellitus.