Under pathological conditions, acquired VAV1 mutations promote lymphomagenesis through multiple mechanisms: enhancing GEF‐dependent RAC1 activation, altering signal transduction via GEF‐independent adaptor functions, and potentially losing tumor suppressor activity, ultimately leading to aberrant follicular helper T cell (Tfh) activation and malignant transformation [6]. The gene discussed is ARHGEF2; the disease is neoplasm.