Krumlauf worked with a variety of renowned scientists in the field of developmental biology throughout his time researching Hox genes.
At the turn of the millennium, Krumlauf came back to the United States to become the founding scientific director of the Stowers Institute for Medical Research.
His research with mutant mouse embryos found that the absence of Hoxb-1 lead to changes in rhombomere 4 (r4) identity.
This mutation causes a difference in migration patterns in r4, which demonstrates that Hoxb-1 is plays a role in the regulation of migratory properties of motor neurons present in the hindbrain.
[6] Krumlauf has manipulated the expression of Hox genes in many ways throughout his career in order to observe variations in development amongst certain animals.
For example, in 2013, Krumlauf and his team configured mutant animals with a double-mutant cluster of HoxA-HoxB genes in their neural crest cells.
This helped Krumlauf to determine the HoxB genes are able to enhance a phenotype that was directly caused by the deletion of a HoxA cluster.
Gnathostomes were used in this research in an attempt to determine how primitive the relationship between Hox gene expression and segmentation of the hindbrain is.
Hox genes control a variety of regulatory interactions in the hindbrain which leads to segmentation in animals.
Krumlauf studied the Hox genes present in chordates and found these invertebrates to lack hindbrain segmentation.
This data demonstrates that gene loss of prototypical Hox clusters is a defining feature in both tetrapod and fish evolution.