Drug resistance is a major obstacle in drug efficacy that causes cancer cells to be insensitive to targeted inhibitor therapies and/or conventional chemotherapeutic agents [1,2]. However, there are two categories of resistance to inhibitor therapies: de novo and acquired [3]. By definition, de novo resistance is a phenotypic characteristic present before drug exposure where drugs with proven efficacy fail to cause tumor cells to respond with any significance [2,4,5]. Acquired resistance refers to a situation where the initial sensitivity of tumor cells to drugs discontinues despite or due to continued consumption [2]. It has been reported that the underlying mechanisms of both types of resistance are related, often due to mutation, loss, or up-regulation of some other important signaling proteins or pathways [2,5]. De novo drug resistance can be determined by assessing the genetic profiles of tumors for 1) oncogenic addictions to proteins or pathways and 2) other possible genetic alterations conferring resistance [2]. Therefore, targeting de novo resistance can enhance drug efficacy and reduce the chance of acquired resistance [5]. Recently, characterizing drug-resistant tumors, and analyzing cell lines that result from the continuous culture of drug-sensitive cells in the presence of an inhibitor have been shown to be successful approaches for identifying changes responsible for acquired resistance [2].