CD3D and severe combined immunodeficiency: In a recent Cell article, McAuley, Kohn et al. showcased proof-of-principle of a promising gene therapy (GT) approach to correct the underlying genetic defect responsible for CD3δ-deficient severe combined immunodeficiency (SCID) using a CRISPR-Cas9-derived adenine-base-editor (ABE).1 This ground-breaking and important study could impact future GTs for monogenic diseases by providing novel tailored therapeutic options (Fig. 1).