It was found that in the kidney, ChREBP was highly expressed in renal proximal tubular cells, and activation of ChREBP in renal proximal tubular cells mediated a significant elevation of hypoxia-inducible factor-1α (HIF-1α), inducing glomerulosclerosis and tubulointerstitial injury 30, 33, 34. Here, MLXIPL is linked to glomerulosclerosis.