Table 1.

Current potentially actionable genetic alterations in SqCC detected by NGS.

Gene	Clinical findings	Note
ERBB	ERBB family mutations in 21.6% of SqCC, non-statistically significant overall survival difference in favor of afatinib vs. erlotinib (LUX-Lung 8 trial)	Difficulties in discerning mixed passenger mutations from real driver ones
FGFR1	Amplification in 20% of SqCC, no correlation between amplification and increased protein expression, better prognosis independent of treatment, no survival benefit in unselected advanced SqCC patients (LUME-Lung 1 trial) in adding the FGFR inhibitor nintedanib to docetaxel in second-line therapy	Role pending in ongoing large international studies
PI3K	Missense mutations and amplifications, in ~20% of advanced SqCC, frequently associated with loss of PTEN, worse prognosis, buparlisib showed poor disease responses with only 20% PFS at 12 weeks among NSCLC patients with PIK3CA activating mutations	Seems not to be a driver mutation

FGFR1, fibroblast growth factor receptor; NGS, next-generation sequencing (NGS); PI3K, phosphatidylinositol 3-kinase; SqCC, squamous cell carcinoma.