Indeed, some studies have shown that the hybrid gene, considered pathognomonic, can be detected only in a minority of FH1 patients, and that the use of plasmids containing a large fragment of the wild-type CYP11B2 gene and the chimeric gene - including segments where the most frequent breakpoints occur - could represent more sensitive tools for the molecular diagnosis of FH1 [66, 67]. This evidence concerns the gene CYP11B2 and glucocorticoid-remediable aldosteronism.