The inactivity of CTLA4 might result in a loss of the inhibition of the signaling pathway of CD86-CD28 which impacts the differentiation of blood cells (Th1 and B cells) but more interesting, the association of CTLA4 with autoimmunity might point towards a hypothesis that lymphoid neoplasms might share the same alterations as autoimmune diseases49. The gene discussed is CD86; the disease is lymphoid neoplasm.