Furthermore, a constitutive podocyte-specific APOL1-expression mouse model (using Nphs1promoter) did not induce overt kidney disease or albuminuria in spite of reduced podocyte density.27 The authors speculated that a combination of podocyte G1-/G2-APOL1 expression, reduced podocyte density, and another upstream hit is required to drive APOL1-mediated FSGS. This evidence concerns the gene APOL1 and kidney disorder.