For example, in FTLD-TDP caused by GRN mutations, the TMEM106B risk haplotype modifies disease risk to such an extent that people who are homozygous for the protective TMEM106B haplotype may remain lifelong symptom free, whereas in Parkinson’s disease and ALS the TMEM106B haplotype association is restricted to an effect on the degree of cognitive decline [36, 51, 67]. This evidence concerns the gene TMEM106B and amyotrophic lateral sclerosis.