Simplifications: the fly bench is a rule based model of the textbook cascade, not a reaction-diffusion simulation. Bicoid fates read one threshold on an exponential gradient (length constant 15% of egg length), and posterior fates are compressed when anterior ones expand. Segment deletions follow the textbook mutant phenotypes at the level of whole segments (real pair rule and segment polarity defects remove parasegment-sized or partial units). The tumor patch uses exaggerated mutation rates, a simple neighbour-replacement model and three driver genes (APC and TP53 need two hits, KRAS one; mismatch repair loss multiplies the mutation rate). The age of onset curve comes from a separate cohort model calibrated so that about 4 to 5 percent of people with no inherited hit develop colorectal cancer by 85; real risks vary by gene, variant and screening.
Type probabilities as a fraction (1/4), a decimal (0.45), a percent (45%) or e-notation (4e-6); answers within about 2% are accepted. Fly problems assume fully penetrant recessive loss of function alleles unless stated. Two hit problems use the Poisson model with independent cells.
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Fictional people and data. Teaching examples only, not medical advice or genetic counseling. Real testing and treatment decisions consider much more information.
Wrong picks are fine here. Each one tells you why.