Other described bypass resistance mechanisms include activation of FGFR2&3 and cMET.29 Interestingly, previous studies have identified and receptor tyrosine kinases (RTK), such as FGFR2, can act as an upstream activator of ERBB3.30 In addition, metabolic reprogramming of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) via STAT3 has recently been linked to ALK TKI resistance.31 Clinical evidence of co-targeting multiple signaling pathways is still missing in ALK translocated NSCLC. The gene discussed is MET; the disease is non-small cell lung carcinoma.