As Smad3 is a key mediator of renal fibrosis 51, it is highly possible that after SARS-CoV-2 infection, intracellular release of SARS-CoV-2 N protein can bind and activate TGF-β/Smad3 signaling to induce the cell death pathway to trigger renal inflammation and “cytokine storm”, resulting in AKI. This evidence concerns the gene TGFB1 and renal fibrosis.