This strategy can correct aberrant gene splicing events and increase the expression of the normal PKHD1 gene, opening up new possibilities for the treatment of ARPKD caused by splicing defects.[43] Enhanced renal c-myc mRNA expression has been observed not only in rodent animal models of PKD but also in human ADPKD patients. The gene discussed is PKHD1; the disease is autosomal recessive polycystic kidney disease.