The potential impact of this loss-of-function mutation was validated by depleting NRXN3 (given the early stop codon mutation detected, which is likely a loss-of-function event) in a naïve PC9 lung cancer cell line, which increased levels of phosphorylated AKT, a previously identified convergent feature of EGFR TKI resistance48, and conferred resistance to EGFR TKI treatment (Extended Data Fig. 9b–d). Here, EGFR is linked to lung cancer.