Kir7.1, an inwardly rectifying potassium channel encoded by the KCNJ13 gene, is a member of the Kir channel family. In 2026, Kir7.1 research advanced rapidly in both structural biology and precision therapeutic development. Multi-state Cryo-EM structures revealed how phosphatidylinositol 4,5-bisphosphate (PIP₂), cholesterol, and bioactive steroids modulate channel conformation; prime editing of the KCNJ13 L144P variant restored channel function; and anticodon-engineered transfer RNA (ACE-tRNA) promoted targeted readthrough of the W53X premature termination codon and improved electroretinographic responses in Leber congenital amaurosis type 16 (LCA16) mouse model [1–3]. Additional structural studies clarified the molecular basis of the R162W loss-of-function phenotype and the pore-blocking mechanism of ML418 [5,10]. Together, these advances position Kir7.1 at the intersection of retinal ion homeostasis, channel structural biology, and precision therapy.