To begin to interrogate the signaling interplay of high IL-17F-expressing Th17 cells with CLL cells and the tumor microenvironment, we performed SCNP analyses in which PBMC samples from CLL patients and healthy donors were incubated in vitro with IL-17F and the evoked signaling in pathways known to be triggered by IL-17F, including NFκB (p105NFkB), PI3K (p-Akt), and MAPK (p-ERK), was quantified. The gene discussed is AKT1; the disease is neoplasm.