cMET (or MET) is a proto-oncogene that encodes the MET receptor tyrosine kinase. cMET gene amplification has long been known as an important resistance mechanism to EGFR-TKIs (tyrosine kinase inhibitor) such as osimertinib, in addition to the appearance of EGFR mutations such as the T790M and del19 mutations. 
Ba/F3 is a murine pro-B cell line frequently used in laboratory research to study the effects of genetic alterations, particularly in the context of oncogenes. In order to screen EGFR-TKI drug and mechanism, Signosis provides the EGFR del19 (746-750) & T790M + cMET expressing Ba/F3 cell line with del19 (746-750) deletion, T790M mutation and cMet overexpression.  The use of such cell lines is crucial for understanding the complex interplay of mutations in cancer cells and for evaluating potential therapeutic strategies.
The cell line was established by electroporation to transfect Ba/F3 cells with 2 separate vectors; one containing EGFR del19 (746-750) & T790M with GFP and hygromycin resistance, and the other with cMET and G418 resistance. Clones with resistance to both hygroymcin and G418 were subsequently screened for GFP expression, with protein expression of both EGFR del19 (746-750) & T790M and cMET tested via western blot. The clone with the highest espression selected and expanded to produce this stable cell line.