Additionally, Nicolai et al. determined that farnesol could reside deeply within the CD1a cleft, adopting a medial alignment and suggesting that haptenation is not essential.43 Similar to urushiol, farnesol was observed to displace endogenous lipids from the CD1a groove, further supporting a hapten-independent model of ACD pathogenesis. The gene discussed is CD1A; the disease is granular corneal dystrophy type II.