Further investigations showed that miR-98 mimetic and MECP2 siRNA reduced the mRNA and protein levels of transient receptor potential 3 (TRPC3), one of the target genes of MECP2 involved in vasoconstriction and the regulation of blood pressure in metabolic syndrome [60], and the miR-98 inhibitor and MECP2 expression vector increased TRPC3 expression. Here, MECP2 is linked to metabolic syndrome.