In the context of NPM1-ALK+ ALCL, ERK1/2 are known to drive proliferation by promoting cyclin-dependent kinase 4 (CDK4) activity and phosphorylation of retinoblastoma protein, and maintaining viability by positively regulating the expression of anti-apoptotic factors (e.g., Bcl-xL); ERK1 rather than ERK2 holds prominence in maintaining cell viability [27]. Here, CDK4 is linked to anaplastic large cell lymphoma.