Although the mechanisms of development of these drug-induced MCNS/FSGS cases are not well understood, the drugs mediate the dysfunction of podocytes to form nephrotic-level proteinuria, and RelA, the master subunit of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kB) and c-mip that induces podocyte disorder, is thought to play a key role here. This evidence concerns the gene NFKB1 and lipoid nephrosis.