In agreement with the presence of off-target mechanisms able to explain the lack of response to TKIs, the resistance to crizotinib in ALCL was also explained by the concomitant downregulation of phosphatases PTPN1 and PTPN2, subsequently leading to the hyperactivation of SHP2, MAPK and JAK/STAT pathways [31]. The gene discussed is SOAT1; the disease is anaplastic large cell lymphoma.