Therefore, it could be speculated that in CS patients, the high circulating miR-133a-3p levels might (1) induce an autocrine catabolic action on skeletal muscles inducing atrophic signalling; (2) induce an endocrine role on brain-specific pathophysiological mechanisms of illness, mainly BD and schizophrenia; and (3) sustain the prolonged GCs effects negatively regulating the post-transcriptional activity of FKBP5. The gene discussed is FKBP5; the disease is Cowden syndrome 1.