EGFR and neoplasm: These observations suggest that: (i) tumor capacity to evolve and adapt to therapy can be inhibited by neutralizing the selective advantage of resistant over sensitive cells; (ii) the capacity of resistant cells to grow in the presence of EGFR-TKIs could represent, by itself, some kind of collateral vulnerability that can be pharmacologically targeted; (iii) since it’s not aimed at a specific mechanism of resistance, an approach directed against this type of vulnerability could be more broadly effective in prolonging the response to EGFR-TKIs.