We used established therapeutic approaches to improve hyperglycemia (SGLT2i and insulin) and observed sustained p21 expression in both cases, supporting the notion that sustained p21 expression reflects the hyperglycemic memory independent of the glucose-lowering intervention and independent of exposure of tubular cells to urinary glucose (which is expected to be increased in SGLT2i-treated, but not insulin-treated mice). The gene discussed is INS; the disease is Hyperglycemia.