A fundamental question promoted by our work is whether experimental HT challenge might mimic parts of a (chronic) pathologic HT exposure, potentially contributing to various neuropathologies in patients/animals39–44, particularly the predicted potential function of TNF-/EGF-signaling components as AMD risk or progression factors1,45–48 (Fig. 10e and Supplementary Data 1). The gene discussed is EGF; the disease is age-related macular degeneration.