Overall, these findings suggest that CAE pre-treatment acts as an effective chemopreventive agent by hindering tumor growth, restoring antioxidant activity, and downregulating survivin expression to normal levels, whereas post-treatment acts as an ideal cancer therapy by inducing tumor shrinkage, upregulating Casp3 and Gsdmd expression, and reducing survivin expression, and at the same time lowering the oxidative stress (Fig. 6). Here, BIRC5 is linked to neoplasm.