For example, the weaker anchor residue Ala2 in the HLA-A*02:01-restricted MART-1/Melan-A25-36 peptide (EAAGIGILTV), which is overexpressed in melanoma, allowed the MEL5 TCR to “pull” the N terminus of the peptide away from the HLA-I groove, facilitating new contacts that were not able to form when the anchor residue was optimised in the heteroclitic ELAGIGILTV peptide [41, 95] (Fig. 2C). The gene discussed is HLA-A; the disease is melanoma.