TUBA4A and neurodegenerative disease: There are only a few known exceptions, including homozygous null and in-frame deletion mutations in TUBβ8 that can cause an oocyte maturation defect [23], a dominant nonsense mutation that results in a slightly truncated TUBα4A linked to the neurodegenerative disease amyotrophic lateral sclerosis [19], and a recessive intron deletion in TUBα8 in polymicrogyria patients that interferes with splicing, producing shorter mRNAs that do not contain exon 2 [24].