In this paper, we describe the anticancer potential of jozimine A2, a naphthylisoquinoline alkaloid, on drug-sensitive CCRF-CEM leukemia cells and provide valuable information regarding its mechanism of action and the difference in activity in comparison to a structurally related but different NIQ alkaloid dimer, namely michellamine B. By using bioinformatic tools, we uncover the binding site that leads to the inhibition of the NF-κB pathway in silico. The gene discussed is NFKB1; the disease is leukemia.