We previously reported that ABCA1 deficiency is one of the peculiarities in glomeruli isolated from patients with T2D and DKD [2], an observation which we further confirmed by demonstrating that genetic or pharmacological overexpression of ABCA1 is sufficient to ameliorate podocyte injury in a mouse model of DKD [16,17]. The gene discussed is ABCA1; the disease is type 2 diabetes mellitus.