Diosmin also used dose‐dependent activity for A431 skin cancer cells, by inducing apoptosis through overexpression of caspase 3, p53, and caspase 9 gene overexpression DNA fragmentation, which caused the downregulation of MMP‐2, 9 (matrix metalloproteinases‐2, 9) and Bcl‐2 genes and also ROS‐mediated mechanisms (Eraslan et al., 2017; Perumal et al., 2018). Here, BCL2 is linked to skin neoplasm.