Da Silva J, Jouida A, Ancel J, et al. - Researchers examined the links between HER2 and the tumour suppressor fragile histidine triad (FHIT) in lung tumour cells, to ultimately refine the target population for anti‐HER2 therapies in non‐small cell lung cancer (NSCLC). In NSCLC samples as well as in lung tumour cell lines, experts identified a negative correlation between FHIT expression and the activated form of HER2 (pHER2). A rise or decline of HER2 activity was caused by the silencing or overexpression of FHIT in lung cell lines, respectively. Irbinitinib and trastuzumab (two anti‐HER2 drugs) were shown to restore a more epithelial phenotype and counteracted cell invasiveness as well as growth of FHIT‐silenced tumour cell lines. In primary tumour cells from NSCLC patients, the sensitivity to an anti‐HER2 therapy was predicted by FHIT^low/pHER2^highphenotype. According to the findings, FHIT was identified as a regulator of the activity of HER2 in lung tumour cells, and sensitivity to HER2 inhibitors was displayed by FHIT‐inactivated tumour cells. The likely eligibility of a novel subclass of NSCLC patients for an anti‐HER2 therapy was also suggested.