This differential influence of HCN channels on synaptic and intrinsic neuronal excitability has implicated HCN plasticity in the vulnerability and resilience to several neurological disorders characterized by abnormal synaptic or intrinsic excitability, such as epilepsy, neuropathic pain, depression, and Parkinson’s disease (Chaplan et al., 2003; Biel et al., 2009; Chan et al., 2011; Emery et al., 2011; Friedman et al., 2014). Here, MALAT1 is linked to epilepsy.