We probed PKA substrate phosphorylation in hearts in response to 8 weeks of TAC and observed normal levels in control hearts but an accumulation of phosphorylated PKA substrates in Rac1cKI hearts (Figure 6, C and D), suggesting Rac1 S-palmitoylation cycling may be necessary to repress sustained PKA activity or to promote dephosphorylation of PKA substrates. This evidence concerns the gene RAC1 and persistent truncus arteriosus.