Finally, ubiquitination assays revealed that USP38 knockout enhanced STRAP ubiquitination, while USP38 overexpression reduced the formation of Ub-STRAP complexes, thereby supporting our hypothesis that USP38 acts as a deubiquitinase that stabilizes STRAP to sustain TGF-β–mediated fibrotic signaling in CKD (Fig. 8I, J). Here, USP38 is linked to chronic kidney disease.