Upon activation through cleavage, it degrades various cellular components, thereby driving apoptosis.[39] As shown in the WB results (Figure 5B–G), expression levels of Bax and Cytosolic‐Cyt c (C‐Cyt c) were significantly upregulated in the kidneys of the AKI group, while the expression of the anti‐apoptotic protein Bcl‐2 was downregulated, indicating the activation of intrinsic apoptosis. The gene discussed is BCL2; the disease is acute kidney injury.