Further, functional analysis of p.Asp316Gly along with five other mutations associated with non-syndromic tooth agenesis showed that this mutation, unlike other five, drastically reduces interaction between EDA receptor (EDAR) and mutant EDA1 protein.[31] These two studies clearly indicate that mutation(s) which severely affect the receptor binding activity of EDA protein may show almost complete penetrance for male and female in spite of the X inactivation. The gene discussed is EDA; the disease is tooth agenesis.