RHOA and progeroid syndrome: The increased F‐actin polymerization and cytoskeletal stiffness in senescent cells could be caused by sustained RhoA activation, which can impair proper actin dynamics and normal cellular function, and further enhance DNA damage, ROS production, nuclear blebbing, cytoplasmic DNA/cGAS‐Sting‐mediated innate immune responses, chromatin dysfunction, and other progeria phenotypes.