While KLF4 strongly promotes SMC de-differentiation by inhibiting the expression of SMC markers (contractile proteins) in vitro and in arteries undergoing IH [16, 17], c-MYB perpetuates SMC proliferation and migration; reducing c-MYB activity hampers IH in arteries and veins in animal models [18–22]. Here, KLF4 is linked to isolated hemihyperplasia.