Notably, following ANGPTL4 knockdown, the level of α-SMA remained greater than that in the control group, indicating that ANGPTL4 may not be the sole regulatory factor in renal fibrosis and that other HIF-1α-mediated regulatory pathways, such as the PI3K/AKT signaling pathway, may also be involved [42]. This evidence concerns the gene ANGPTL4 and renal fibrosis.