Mean BP elevations by Ang II were significant as compared with the corresponding mice assessed prior to the Ang II infusion but yielded no gross differences between both genotypes (Figure 1F and G, S4K), suggesting that the higher susceptibility of CMF-specific cGKI KO hearts is due to local, i.e., intra-cardiac effects of the neurohormone Ang II, which promotes, besides its other adverse actions, the pro-fibrotic signaling in CF/CMF [86,87]. Here, PRKG1 is linked to cystic fibrosis.