Nevertheless, PI3K inhibitor monotherapy results in a low frequency of complete responses, and patients treated with the PI3K inhibitor idelalisib eventually develop resistance owing to activation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and mTOR (mammalian/mechanistic target of rapamycin) pathways in activated B cell-like diffuse large B-cell lymphoma (ABC DLBCL) [14–16]. This evidence concerns the gene NFKB1 and diffuse large B-cell lymphoma.