Resistance to tyrosine kinase inhibitors of ALK has been described in multiple tumor types and can arise through different mechanisms.1 Here we show that in ALKF1174L-driven NB cells, the development of resistance to TAE684 and its clinically available derivative, LDK378, is associated with AXL overexpression and activation, as well as increased ERK signaling. Here, ALK is linked to neoplasm.