HSPB8 and melanoma: The mutant W51C HSPB8 acquires a predicted different secondary structure characterized by seven additional β-turns [40] and, in this way, is capable of altering HSPB8 protein–protein interaction, conferring a dominant anti-apoptotic activity to the mutated protein [40]; this greatly differs from the typical pro-apoptotic activity of wtHSPB8 in melanoma cells.