Proteins are the molecular machines that drive almost every biological process in living organisms. The correct folding of a protein is crucial for its function, as its three-dimensional structure determines its biochemical properties and interactions with other molecules. However, protein folding is not always perfect. Misfolding or incomplete folding can lead to dysfunctional proteins, which is implicated in various diseases. One of the most significant classes of diseases caused by protein misfolding are textit{channelopathies}, disorders that involve ion channel dysfunction, often due to the misfolding of ion channel proteins.This article delves into the kinetics of protein folding, explores the mathematical models that describe the folding process, and investigates how anomalies in folding kinetics contribute to the pathophysiology of channelopathies. The article covers the physical principles behind protein folding, the influence of mutations on folding dynamics, and how disruptions in folding kinetics lead to misfolded ion channel proteins, causing diseases such as cystic fibrosis, epilepsy, and certain cardiac arrhythmias.