A recent study indicated that tubular damage and atrophy can actively promote a pro‐inflammatory state and sustained myofibroblast recruitment during the AKI‐to‐CKD transition, mediated via VCAM‐1.[38] However, our findings may challenge this mechanism in the context of SH045‐induced nephroprotection, as VCAM‐1 expression was paradoxically elevated in the SH045‐treated group (fold change: 0.36) (Table S1, Supporting Information). The gene discussed is VCAM1; the disease is chronic kidney disease.