Immunoprecipitation assays showed that pressure overload decreases the physical interaction between Bcl-xL and IP3R-type 2 in WT mouse hearts, but not S14A knock-in mouse hearts, in the presence of TAC (Fig. 5c), suggesting that Ser14 phosphorylation during TAC inhibits Bcl-xL-IP3R interaction. Here, BCL2L1 is linked to persistent truncus arteriosus.