Lv et al. (2020) have originally found that sEV-miR-19b-3p derived from TECs facilitated M2 macrophage activation via targeting the NF-κB/suppressor of cytokine signaling 1 (SOCS-1) in LPS-induced AKI. Another study in China discovered that sEV-derived miR-155 promoted the progression of AKI by mediating communication between activated macrophages and damaged tubules. The results of all of these studies have contributed to our understanding of AKI’s pathophysiology (Zhang et al., 2022). Here, SOCS1 is linked to acute kidney injury.