SMN2 and proximal spinal muscular atrophy: 2021). Homozygous absence of SMN1 exon 7 and retention of exon 8 in type I patients has been postulated to be the result of unequal crossing over, while that found in types II and III has been considered the result of SMN1 gene conversion into SMN2 (Kekou et al. 2020).  Gene conversion events have been reported to account for the minority of SMA patients with a frequency of 3–28% (Yuan and Jiang. 2015).