MYH9 and glomerulosclerosis: In this report we have extended our analysis of Myh9 function in the podocyte in vivo in two areas: first, if PodΔMyh9 on the C57BL/6 background has no overt phenotype but the same deletion on a mixed background results in spontaneous and severe glomerulosclerosis, we hypothesized that mouse congenics could identify the genetic loci responsible for this strain specific resistance or sensitivity to PodΔMyh9.