As predicted by TPMS analyses (Figure 2), brigatinib targets appear to show a more diverse range of effects compared to alectinib, mediated by ALK inhibition on NSCLC, such as: cell growth and proliferation (as for example STAT3 [78], PI3K [79], K-Ras [78, 80] or erbB2 [81] signaling); evading apoptosis (through EGFR-CASP3 interplay [82]); acting over sustained angiogenesis (IGF1R signaling [83, 84]); and tissue invasion and metastasis processes (modulating the E-cadherin-β-catenin axis [85–88]). This evidence concerns the gene IGF1R and non-small cell lung carcinoma.