Besides, given the complexity of kinase interrelations and dynamics, the use of kinase inhibitors targeting one single kinase usually results in the acquisition of resistance to such treatments [43] or even in the overexpression of PD-L1 as a result of the activation of alternate networks leading to STAT3 and ERK1/2 stimulation [130], a phenomenon that has already been reported in resistant non-small cell lung cancer [130] and that makes necessary a thorough preliminary proteomic study of patients in order to choose the more appropriate inhibitor combinations. Here, STAT3 is linked to non-small cell lung carcinoma.