BCR co-receptor CD19 and the BCR itself (through SYK kinase) are able to activate PI3K signaling, which leads to activation of AKT which activates downstream mTOR promoting cell survival, again showing the large role BCR signaling plays in promotion of DLBCL (Uddin et al., 2006; Young and Staudt, 2013). This evidence concerns the gene AKT1 and diffuse large B-cell lymphoma.