The phenotypic transition has been related to three mechanisms: first, an increase in PCSK1 and PC1/3 expression has been reported in three cases of SCAs that evolved during follow-up to functioning ones, thus underscoring the role of PC1/3 as one of the most feasible mechanism for silencing corticotroph adenomas [39]. This evidence concerns the gene PCSK1 and ACTH-producing pituitary gland adenoma.