Early research indicates that increased autophagy contributes to the progression of PDAC because genetic (e.g. atg7-/- or hmgb1-/-) and pharmacological (e.g. using CQ) inhibition of autophagy results in the production of reactive oxygen species (ROS), increased DNA damage and metabolic dysfunction, which ultimately prevents the development of PC in vitro and in vivo [75,76]. Here, ATG7 is linked to pachyonychia congenita.