This hypothesis is supported by laboratory evidence (higher growth of bacteria on textured implants both in vitro and in vivo [5], linear increase in lymphocyte activation proportional to bacterial load [6], detection of bacterial species with shift in the microbiome towards the Gram-negative spectrum in BIA-ALCL specimens [7], accumulation of JAK1 and STAT3 mutations in patients with BIA-ALCL [8]) and epidemiological evidence (up to 23 times higher risk of BIA-ALCL for implants with high surface area that supports higher rates of bacterial growth in vivo [3,9]). This evidence concerns the gene JAK1 and anaplastic large cell lymphoma.