Consistent with this possibility, results of expression studies confirmed that cells expressing CMT/FSGS variants indeed had more prominent cytoskeletal disarrangement and organelle perturbation compared to FSGS INF2 variants, and the disorder associated with the CMT/FSGS variant would exceed the critical threshold to trigger disease in both Schwann cells and podocytes (Fig. 13). The gene discussed is INF2; the disease is focal segmental glomerulosclerosis.