Based on current research, DMD develops due to open-reading frame disruption or dystrophin mRNA alteration caused by exon deletion or mutations.65,66 CLK1-regulated splicing manipulation, especially the exon-skipping function, was reported to contribute to DMD.67 A patient harbored c.4303 G > T point mutation in dystrophin gene exon 31 changed SRp30c/SRSF9-dependent exon skipping enhancer (ESE) to hnRNP A1-dependent exon skipping silencer (ESS), thus, leading to exon 31 skipping to generate truncated, but functional dystrophin protein. Here, DMD is linked to Duchenne muscular dystrophy.