Takeda et al.[19] reported that PC hyposialylation or desialylation in rats, generated by treatment with reagents such as puromycin aminonucleoside, disrupts PC complexes containing PC, NHERF2 and ezrin, and their interactions with the actin cytoskeleton, resulting in a loss of foot processes similar to that seen in human nephrotic syndrome. This evidence concerns the gene NHERF2 and nephrotic syndrome.