Neuronal ceroid lipofuscinosis (NCL) is a group of autosomal recessive diseases characterized by blindness, loss of cognitive and motor function, and early death. One of the genes that is mutated in this disease is CLN3. When functional CLN3 protein is absent, neurons die because of increased storage material in the cells, presumably because the lysosomes aren't working properly. What is a valid explanation as to why parents of children with this devastating disease can be unaffected?

(A) Parents of the autosomal recessive disease must both be carriers of the mutation on the CLN3 gene.
(B) Carriers of the CLN3 mutation genotype do not show the phenotype because one normal CLN3 allele is present to provide a functioning CLN3 protein.
(C) Redundant proteins take over the function of the mutant CLN3 protein in the parents.
(D) X inactivation prevents expression of the CLN3 mutated protein in the parents.