In contrast to the findings in global KO mice, podocyte-specific KO of only GSK3 β or GSK3α in mice either at the embryonic stage or during young adulthood resulted in no discernible phenotype, whereas combined KO of both GSK3α and GSK3β specifically in glomerular podocytes in embryonic or adult mice caused severe podocyte injury, glomerulosclerosis, heavy proteinuria, and significant impairment of kidney function [24]. This evidence concerns the gene GSK3A and glomerulosclerosis.