Disrupting the 3′ splice site via adenine‐to‐guanine (A‐to‐G) conversion can induce exon skipping (Figure5a), a strategy that may reduce the expression of pathogenic proteins.[35] We engineered endCas12j‐8‐ABE editors to target the SOD1 (associated with Amyotrophic Lateral Sclerosis, ALS)[36] exon 3 3′ splice site using a TTA PAM‐specific crRNA. Here, SOD1 is linked to amyotrophic lateral sclerosis.