Additionally, an experimental study suggested that HBx directly upregulated the expression of lncNBAT1, which can interact with STAT1 to prevent its enrichment at the promoter region of the functional target gene apolipoprotein B mRNA editing enzyme catalytic subunit 3A (APOBEC3A), inhibiting the expression of APOBEC3A and inducing resistance to MTX in DLBCL cells (24). This evidence concerns the gene APOBEC3A and diffuse large B-cell lymphoma.