While focusing on the important COVID-19 targets ACE2 and TMPRSS2 molecules, we re-analyzed these data sets and confirmed that our approach was valid when we identified 3 previously known candidates of lung-kidney cross-talk during AKI: lipocalin 2 (NGAL), suppressor of cytokine signaling 3 (member of STAT family), and inhibin beta B. NGAL is a bio-marker of AKI but also has important role in iron metabolism, epithelial cell and immune cell functions. Here, SOCS3 is linked to COVID-19.