CDKN2A and neoplasm: Second, intrinsic cellular differences may also contribute, with female cells potentially relying more on Cdkn2a/p16‐mediated senescence as a tumor‐suppressive mechanism, whereas male cells may preferentially accumulate DNA damage, leading to apoptosis or transformation.[74, 75] These findings are consistent with prior work showing sex‐dependent variation in senescent cell burden.[37]