However, the authors speculated that compromised interaction of INF2 with actin/CAP complexes may contribute to the mechanisms underlying human diseases such as focal segmental glomerulosclerosis and Charcot-Marie-Tooth [2], which both have been linked to dominant missense mutations in INF2’s DID that reportedly binds CAPs with sub-micromolar affinity [1, 2, 8, 10]. Here, CAP1 is linked to focal segmental glomerulosclerosis.