Even though targeted therapies have increased the life expectancy of patients with druggable driver alterations [53], their efficacy could be limited when tumor cells acquiree therapy resistance mutations, which, depending on the resistance mechanism used, could impact the same molecular target (On-target), MET parallel tyrosine kinase signaling, or its own signaling pathways with the aim of treatment breakdown [54,55], so, the knowledge about the driver’s signaling pathways alterations will be relevant to predicting the possible drug bypasses at diagnosis [56]. Here, MET is linked to neoplasm.