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<i>LMNA</i>-related muscular dystrophy is an autosomal-dominant progressive disorder caused by mutations in <i>LMNA</i>. <i>LMNA</i> missense mutations are becoming correctable with CRISPR/Cas9-derived tools. Evaluating the functional recovery of <i>LMNA</i> after gene editing bears challenges as there is no reported direct loss of function of lamin A/C proteins in patient-derived cells. The proteins encoded by <i>LMNA</i> are lamins A/C, important ubiquitous nuclear envelope proteins but absent in pluripotent stem cells. We induced lamin A/C expression in induced pluripotent stem cells (iPSCs) of two patients with <i>LMNA</i>-related muscular dystrophy, NM_170707.4 (<i>LMNA</i>): c.1366A > G, p.(Asn456Asp) and c.1494G > T, p.(Trp498Cys), using a short three-day, serum-induced differentiation protocol and analyzed expression profiles of co-regulated genes, examples being <i>COL1A2</i> and <i>S100A6</i>. We then performed precise gene editing of <i>LMNA</i> c.1366A > G using the near-PAMless (PAM: protospacer-adjacent motif) cytosine base editor. We show that the mutation can be repaired to 100% efficiency in individual iPSC clones. The fast differentiation protocol provided a functional readout and demonstrated increased lamin A/C expression as well as normalized expression of co-regulated genes. Collectively, our findings demonstrate the power of CRISPR/Cas9-mediated gene correction and effective outcome measures in a disease with, so far, little perspective on therapies.