The pathophysiological mechanisms underlying FSGS may be different from case to case, ranging from nonspecific podocyte injury to abnormal immune response (probably in our patient) with production of CLCF-1 or anti-CD40 antibodies and suPAR and up to podocyte expression of molecules including B7-1, B7-2, and CD40. Here, CD86 is linked to focal segmental glomerulosclerosis.