KRAS and small cell lung carcinoma: The molecular mechanisms driving resistance to osimertinib are diverse and may involve EGFR-dependent (e.g., C797S, L718Q, or G724S mutations) or EGFR-independent mechanisms and bypass track mechanisms, such as MET amplification, HER2 amplification, PIK3CA mutations, BRAF mutations, KRAS mutations, and histologic transformation to small-cell lung cancer (SCLC) (6–8).