Researchers developed a novel bionformatic method to identify genes that commonly are regulated by the corrector drugs of CFTR-F508del protein. 47 genes resulted involved in controlling proteostasis of the mutated protein and highlighted 8 signaling pathways/ networks. One of these pathway was deeply characterized and the protein MLK3 appeared to be the central component. The mechanism of MLK3 was investigated and it was found to control the endoplasmatic reticulum associated degradation of CFTR-F508del and also the plasma membrane quality control of CFTR-F508del. Additionally, small molecules mediated inhibition of the MLK3 pathway was observed to rescue CFTR-F508del and thus suggesting a potential pharmacological approach.