Based on this evidence, we hypothesized that defects in PRKG1 activity in smooth muscle cells might promote the alteration of contractile function, resembling the pathophysiological aspects of achalasia disease, and the observed inverse correlation between the miR-200c-3p and PRKG1 (both at transcriptional and translational level) emphasizes its possible involvement in the pathogenesis and development of achalasia. The gene discussed is PRKG1; the disease is Achalasia.