Targeting LRNA9884 effectively blocks MCP-1-dependent renal inflammation, and Smad3 interactions or Smad3-dependent interactions between LRNA9884 and MCP-1 may be an additional mechanism by which Smad3 deletion in db/db mice suppresses renal inflammation in diabetic nephropathy [59, 60]. Here, SMAD3 is linked to diabetic kidney disease.