Increased expression of high affinity HSPG binding sites for bFGF reported in the renal interstitium during tubulointerstitial fibrosis (33) may provide an additional mechanism for strongly inhibitory or FGF-like stimulatory autoantibodies to differentially modulate the rate of tubulointerstitial fibrosis thereby slowing or accelerating, respectively, the rate of decline in renal function in diabetic nephropathy. The gene discussed is FGF2; the disease is diabetic kidney disease.