Since EGFR [20], BRAF [21], ERBB2 [22], MET [23,24] and the EML4-ALK translocation product [8] are clients of HSP90, acting as oncodrivers in different clinico-pathological subsets of lung adenocarcinoma, degradation of these oncoproteins through HSP90 inhibition leads to loss of tumor-cell viability [25,26,27,28]. Here, ALK is linked to lung adenocarcinoma.