There KIT oncogene tends to be dominant, but remember that dominance
depends on the RELATIONSHIP BETWEEN TWO ALLELES, so it entirely possible
for an allele to be dominant to something and recessive to something
else, just as a person may exert power over one individual but take
orders from another one.  Some are strongly dominant, some strongly
recessive, but it always depends on what combination the individual
inherits.  To top it off sometimes there are variations of some alleles,
and sometimes the expression is very dependent on the actions of alleles
in other genetic locations which may either supress or enhance their
actions.  Sometimes even environmental factors play in.  A family which
is normally quite resistant to malignancies may still wind up with them
if smoking or eating a lot of animal fat is common.  A child who was
undernourished when young may have the genotype (the genetic alleles)
for being tall but will wind up stunted, so that individual has a tall
genotype but wound up with a short phenotype.  You can think of enough
examples to fill a page, I would suspect.
 
Remember, too, that some genetic messes are a LOT harder to get out of
then they were to get into.  This is one of them.  It is better avoided
in nations where people are intelligent enough to learn through reading
rather than through experience trouble first hand.
 
An example of studies on KIT oncogene which mention dominance (and there
are a lot):
Development. 1996 Nov;122(11):3597-605.
The dominant white spotting oncogene allele Kit(W-42J) exacerbates
XY(DOM) sex reversal.     Nagamine CM, Carlisle C.
 
but then also consider:
 
: Genes Cells.  1998 Apr;3(4):235-44.  recessive spotting: a linked
locus that interacts with W/Kit but is not allelic.  Bennett DC, Trayner
ID, Piao X, Easty DJ, Kluppel M, Alexander WS, Wagner EF, Bernstein A.
 
BACKGROUND: The murine coat-colour mutation recessive spotting (rs) maps
very closely to the W/Kit locus, encoding the proto-oncoprotein Kit, the
protein tyrosine kinase receptor for stem cell factor.  Kit is important
in the development of melanocytes, germ cells, interstitial cells of
Cajal (ICC) and haemopoietic lineages, including mast cells.  rs has
never been genetically separated from Kit, and interacts with Kit
mutations, suggesting that it is a recessive allele of Kit.  Here we have
tested this possibility...
 
so as you can see there are not only relationships to consider but also
variations of the alleles.
 
The concept of variable expression is essential to understanding neural
crest genetics and why it will be so hard to reduce the proportion even
though we should still try, and why nations where this morass has not yet
been created the ferret clubs need to educate, educate, educate to stop
people from breeding ferrets with such markings.  It is harder to
get out of this increase in the proportion of these alleles than it
was to get into it.
 
In variable expression the phenotype varies and the degree to which the
allele expresses itself varies among individuals WHO HAVE THE EXACT SAME
ALLELE.  This is because the action of that genetic variant is on early
fetal cells which have not yet differentiated.  So, let's just take a
situation in which the individuals have not inherited the alleles in
multiple numbers, and has not inherited alleles at other loci (genetic
locations) which also cause neural crest variations.  Okay, one
individual with the allele may have outward signs suppressed, another may
have them show up in part or to some degree, yet a third may be suffering
badly due to having a phenotype which expresses the neural crest variant
genotype strongly.  The kits of the first will NOT have any genetic
benefit over the kits of the third.  They have the allele, so a parent
who looks okay can have offspring whose lives will pay badly for that
allele.
 
Then top it off with this bit of reality: our ferrets may be dealing
with more than one type of neural crest genetic variant, and there are
multiple loci (genetic locations) in which such mutations can cause
neural crest medical disorders (for instance there are at least 5 ways to
cause Waardensburg Syndrome in mammals).  This means that a ferret can
wind up with multiple neural crest causes which have been increased in
the population through breeding for appearance.  Having multiple causes
in one individual may increase the phenotypic results, too.
[Posted in FML issue 4670]