What would happen if there were no SOX9 in an XY human?
Quoting the abstract of this paper verbatim:


  Sox9 is an Sry-box-containing gene that encodes a transcriptional
  activator. During mouse gonadogenesis, Sox9 is detected in the male
  gonad at 11.5 days postcoitus (dpc). At 12.5 dpc, testicular cords
  form, morphologically distinguishing the male gonad from the ovary.
  From this stage onwards, Sox9 expression is restricted to the Sertoli
  cell lineage and persists in the adult. Humans with heterozygous
  mutations in SOX9 develop a skeletal syndrome known as campomelic
  dysplasia. Furthermore, most XY SOX9 heterozygotes show variable
  male-to-female sex reversal, implicating SOX9 in testis development.
  Sox9 heterozygous knockout mice die at birth with a syndrome similar
  to that of human campomelic dysplasia. In contrast to humans, XY
  Sox9+/- mice form normal appearing testes. Germ-line knockout of Sox9
  using a conditional null allele provides a tool for generating Sox9-/-
  mice by simple genetic crosses. However, Sox9-/- mice die soon after
  11.5 dpc because of cardiovascular defects. In vitro culture of the urogenital ridges of XY Sox9-/- results in gonads lacking testicular
  cords and Sertoli cell marker expression, but with the expression of
  ovarian-specific markers. Therefore, Sox9 is essential for diverting
  an intrinsically ovarian program of organogenesis toward testis
  formation.


From MGI page on Sox9:


  Null mutant heterozygotes and conditional knockout mutants display
  perinatal lethality with cleft palate, hypoplasia and distortion of
  numerous cartilage-derived skeletal structures, and premature
  mineralization in many bones. Specific conditional knockout mutations
  are sex-reversed.