It’s good to get a perspective from someone outside of the field. I’d especially appreciate it if you looked at the other thread and offered your opinion on its clarity:
As someone who has done both protein engineering and studied the activities of pathogenic mutants, the latter in inherited cardiomyopathies, I’d say that focusing on nylonase obscures oodles of other relevant data.
For example, in inherited cardiomyopathies, when a new mutant (changing a single amino-acid residue in one of the muscle proteins) is characterized after a teenager dies on the basketball court or the soccer field of hypertrophy and sudden cardiac death, the half of her/his family subsequently found to be carrying the mutant allele is usually normal or subclinically abnormal. So one person’s lethal mutation is her brother’s asymptomatic polymorphism. There’s no bright white line.
The bottom line (mixing line metaphors) is that there’s a lot of wiggle room, even for the complex, highly adaptive, and fast mechanism of cardiac muscle.
Does that make sense?