Our research aimed to model primary hyperoxaluria type 1 in vitro using a stem cell model and assess the potential of adenine base editors in correcting the most common pathogenic AGXT genetic variant, c.508G>A (Gly170Arg), which leads to oxalate accumulation due to alanine‐glyoxylate aminotransferase mislocalization. The gene discussed is AGXT; the disease is primary hyperoxaluria type 1.