With the aim of maximizing the anti-tumor activity of TCR JDI for possible immunotherapeutic applications, phage display was used to engineer a variant (JDIa41b1) with a 106-fold affinity improvement (KD = 0.7 pM) over the parental TCR that retained the ability to distinguish KRASG12D from wild-type KRAS, although JDIa41b1 did acquire measurable affinity for KRAS–HLA-A*11 (KD = 3 μM). The gene discussed is KRAS; the disease is neoplasm.