HCN2 and chronic obstructive pulmonary disease: Xiao et al. demonstrated that gene-specific miRNA mimics, designed to target the 3′ untranslated regions (3′ UTRs) of HCN2 and HCN4, determined the abrogation of the function of these two channels, while miRNA-masking antisense significantly increased HCN2/HCN4 expression and function, providing possible novel gene therapy strategies for cardiac arrhythmias [39].