Our current working model is that the transition from compensated obesity (pre-diabetes, normoglycemia) to decompensated obesity (T2D, hyperglycemia) reflects, among other things, a relative reduction in SWELL1-dependent signaling in peripheral insulin-sensitive tissues30,33 and in pancreatic β-cells58,59— metabolically phenocopying SWELL1-loss-of-function models24,26–30. The gene discussed is INS; the disease is obesity disorder.