At least in the case of Cystic Fibrosis it happens that a mutant protein (which could actually function!) is held in the ER because the ER detects it as misfolded. Does this happen in every type of mutant protein?
If so, should I conclude that such genetic disorders are caused because of the total absence of a protein rather than because of a misfolded protein? If not, why would the ER or anything else in the cell allow some mutated proteins to do any job (Like in the case of Sickle cell anaemia, where an amino acid substitution happens)?
How do scientists conclude that a misfolded protein could have done a good enough job (Like in the case of cystic fibrosis)?