The correct answer is B. Cellular proliferation.
The presence of facial angiofibromas, developmental disability, and seizure disorder is consistent with a syndrome—most notably tuberous sclerosis. This disease is based on a mutation in the TSC1 and TSC2 genes that encode hamartin and tuberin. These two tumor suppressor genes function to control cellular proliferation and growth; thus once mutated, there is proliferation to lead to many of the sequelae of tuberous sclerosis, such as hamartomas.
Although there are a variety of genetic mutations in tuberous sclerosis and other genetic diseases that may be related to cellular metabolism, intercellular transport, nutrient storage, and structural support of the cell, these are less likely to be associated with tuberous sclerosis, as in the case of this patient.
References: Jozwiak J. Hamartin and tuberin: working together for tumour suppression. Int J Cancer. 2006;118(1):1-5. doi:10.1002/ijc.21542