I've been reading a little about the "two-hit" hypothesis for tumor suppressor genes here, which mentions that some genes exhibiting haploinsufficiency are exceptions to the hypothesis. I've read elsewhere on this site (namely the answer to this question) that suggests haplosufficiency as a means of "silencing" the mutation of the tumor suppressor gene such that the expression of the wild-type allele compensates for the mutant allele.
Are there any other mechanisms that contribute to incomplete penetrance of tumor suppressor mutations?