This finding suggests that miR146a-5p levels in vivo might not be as high as levels of upregulated miR146a-5p in vitro to suppress ICAM-1 and VCAM-1 and other mechanisms might be more effective in regulating ICAM-1 and VCAM-1 expression, and elevation of miR146a-5p might result from the inflammatory milieu in OSA patients or from a compensatory response. Here, ICAM1 is linked to obstructive sleep apnea syndrome.