Studies by Ko et al. (2004)suggest mutual stimulatory interactions between SLC26A3, ANO1, and CFTR involve the R region of CFTR and the STAS domain of A6, potentially influencing CFTR gating. This may explain how PKA-induced CFTR stimulation can generate tissue-specific secretory products, and diverse transport phenotypes when CFTR is absent or impaired, as in CF (Frizzell and Hanrahan, 2012). The gene discussed is SLC26A3; the disease is cystic fibrosis.