Indeed, one of the H11/HspB8 missense mutants, W51C, causes anchorage-independent growth and it overrides the death-inducing capacity of the wild-type H11/HspB8 (Figure 3(c)) through activation of the B-Raf/MEK/ERK pathway [36], which is a notorious contributor to melanoma development. The gene discussed is HSPB8; the disease is melanoma.