ALK+ anaplastic large cell lymphoma (ALCL). frequently carries the t(2;5).(p23;q35). resulting in expression of NPM-ALK oncogenic kinase, which is capable of activating multiple oncogenic pathways. ALK+ ALCL is also characterized by overexpression of CD30 receptor, a member of the tumor necrosis factor (TNF). receptor superfamily, which has been targeted for therapy using conjugated anti-CD30 antibodies with clinical success. Also, the tumor suppressor p53 is frequently non-mutated in ALK+ ALCL allowing for therapeutic modulation of p53 reactivation in this lymphoma type. Therefore, this review is focused on the role of CD30 receptor and p53 as novel targets for therapy in ALK+ ALCL, and also provides an update on their potential involvement in ALK+ ALCL pathogenesis.