As a common arrhythmia associated with AVN defects, AV blocks can be subdivided into first-, second-, and third-degree AV block according to the severity of the blockade.13 Considering the notable reduction in PR intervals in rat hearts following the knockdown of Gabrb2 or Slc32a1 (Figs. 6a, b, 7c, d), we speculated that Gabrb2 and Slc32a1 may be effective targets to prevent AV block occurrence or terminate AV block development by recovering normal conduction of the AVN. The gene discussed is SLC32A1; the disease is avascular necrosis.