Beyond genetic models of βIV-spectrin deficiency (qv4J and βIVifKO), we sought to test whether βIV-spectrin phosphorylation at Ser2250/2254 influenced CF phenotype under pathophysiological stress conditions involving AngII treatment, which alters CF phenotype (including increased proliferation) in part through activation of CaMKII (14, 15, 16, 17, 18). The gene discussed is AGT; the disease is cystic fibrosis.