This phenomenon probably derives from the increased expression of nr3c1 mRNA in mutants compared to WT since, as reported by Faught and Vijayan [32] with their mrca402 zebrafish KO line, the lack of Mr does not lead to hypercortisolemia, a feature that is further confirmed in the mria32 line, where the levels of expression of pomca are not affected in mr mutants compared to wild type siblings (Figure S2B). The gene discussed is NR3C2; the disease is adrenal gland hyperfunction.