ALK phosphorylates IGF-1R at the C-terminal Y338 residue; in turn, IGF-1R increases the phosphorylation of ALK and its downstream effectors and promotes the survival of ALK+ ALCL cells by increasing the expression of anti-apoptotic proteins (myeloid cell leukemia [Mcl]-1, Bcl-2, Bcl-xl, etc) (63). Here, BCL2 is linked to anaplastic large cell lymphoma.