As earlier reports suggest that mutations in TP53 may induce resistance through different mechanisms in the cancer cell [61], further classification of distinct TP53 mutation subtypes (e.g., disruptive vs. non-disruptive, missense vs. non-missense, at primary vs. metastatic lesions), both alone and in combination with other EGFR mutation subtypes (e.g., EGFR exon 20 T790M, the most common mechanism of resistance for 1st and 2nd generation EGFR-TKIs), may predict more precisely the impact of TP53 co-mutation on prognosis and survival on EGFR-TKIs. The gene discussed is EGFR; the disease is cancer.