In contrast, fitting the steady‐state activation data with the Boltzmann equation revealed hyperpolarization of the half‐activation potential by 10 mV in CTZ‐induced neurons (40.8 ± 1.7 mV, n = 12) compared to the control group (−30.9 ± 1.8 mV, n = 9; p = 0.0061); however, similar to anti‐PD‐1 antibody treatment, intracellular SSG application did not alter this change in epilepsy‐related sodium channel steady‐state activation (41.7 ± 2.6 mV, n = 11) (Figure 5F). The gene discussed is PDCD1; the disease is epilepsy.