Though the mechanism for such an effect remains to be elucidated, a preliminary study of 23 COVID-19-positive inpatients suggests that subclinical AKI may be common in patients with COVID-19, as determined by elevated levels of the product of urinary biomarker tissue inhibitors of metalloproteinases-2 and insulin-like growth factor binding protein 7 ([TIMP-2] • [IGFBP7]) without significant change in serum creatinine [24]. The gene discussed is TIMP2; the disease is acute kidney injury.