The pathogenesis of HMS is still not fully understood, yet there seems to be agreement consensus on the hypothesis postulated earlier by Fakunle and Ziegler that HMS pathogenesis results from IgM overproduction due to B lymphocytes stimulation by malaria antigen/mitogen [7, 8] as being the basis for the development of HMS. The gene discussed is CD40LG; the disease is Haim-Munk syndrome.