“…Conditions which have been hypothesized as local triggers of chronic inflammation include bacterial contamination, shell shedding of particulates, shell surface friction, and implant-associated reactive compounds [ 28 , [36] , [37] , [38] , [39] ]. Regardless of the primary triggers, chronic inflammation could represent the determining factor driving lymphomagenesis by favoring the accumulation of malignancy-promoting mutations into the chronically stimulated T cells [ [40] , [41] , [42] , [43] , [44] , [45] , [46] ]. To date, there is no general agreement to exclude any of these factors or on how they cooperate in the pathogenesis of BIA-ALCL.…”