A very recent study found that inhibiting exosomal secretion in PTECs by knocking out Rab27a (a key exosome regulatory gene) could inhibit the excessive inflammatory response in PTECs through the miR‐26a‐5p/CHAC1/NF‐kB pathway, thereby delaying the progression of diabetic kidney disease,21 and another study reported similar findings, that inhibiting IRF‐1/Rab27a mediated exosome secretion accelerated albumin degradation, which could reverse tubule injury with albumin overload, and alleviate tubular inflammation by suppressing lysosomal degradation.22 The gene discussed is NFKB1; the disease is diabetic kidney disease.