The present results demonstrate that (i) LINK-A expression was elevated in Ibrutinib-resistant MCL cell lines; (ii) LINK-A enhanced cell viability and repressed Ibrutinib-induced cell apoptosis; (iii) LINK-A enhanced Bcl2 expression in the presence of Ibrutinib; (iv) LINK-A increased Bcl2 expression by activating AKT signaling. Here, AKT1 is linked to mantle cell lymphoma.