Genetic causes of autosomal dominant forms of FSGS/SRNS include mutations in molecules associated with cytoskeletal organization of podocytes [actinin alpha 4 (ACTN4), inverted formin 2 (INF2), anillin (ANLN), and Rho GTPase Activating Protein 24 (ARHGAP24), SD proteins [transient receptor potential cation channel subfamily C member 6 (TRPC6)], and transcription factors [Wilms tumor 1 (WT1) and LIM homeobox transcription factor 1 beta (LMX1B)]. Here, LMX1B is linked to focal segmental glomerulosclerosis.