The scarcity of additional genetic alterations is presumably an important reason why TP53 mutations have a major effect on the clinical phenotype of ALK+ NSCLC: they are associated with increased disease aggressiveness and metastatic dissemination synergistically with EML4-ALK V3, and they are linked with shorter PFS under TKI and shorter OS independently from EML4-ALK V3, so that double positive V3+TP53+ patients have a very high risk of death with a median OS of around 2 years in our series (Table 1) [18]. The gene discussed is TP53; the disease is non-small cell lung carcinoma.