The main cause of FSGS in our patient may be related to the APOL1 polymorphism known to be associated with a higher risk of FSGS.[12] Nevertheless, Dingli et al described a cohort of 13 patients with apparent “idiopathic” FSGS and plasma cell disorders.[13] A close pathophysiological relationship between these 2 entities was suggested, because of the significant improvement in proteinuria observed on chemotherapy, together with the remission of plasma cell disorders in 4 patients with MM.[13] In our patient, the main cause of the FSGS lesions remains hypothetical. This evidence concerns the gene APOL1 and focal segmental glomerulosclerosis.