Cellular senescence suppresses cancer by arresting cell proliferation, essentially permanently, in response to oncogenic stimuli, including genotoxic stress.

Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries have extended its known role to complex biological processes such as development, tissue repair, ageing and age-related disorders.

This finding confirms the well-established pathogenic role of MHC polymorphisms in the development of diverse autoimmune diseases. Therefore, while the association of the MHC locus with autoimmune diseases is not surprising, this finding serves as a positive control for the analysis.