This formation of sclerotic tissue is driven by three primary mechanisms: first, the upregulation of miR-155, which leads to the downregulation of tumour suppressor genes such as FOXO3 and CDKN1B, thereby promoting fibroblast proliferation; second, galectin-7, a pro-apoptotic keratinocyte protein, inhibits fibroblast growth while paradoxically increasing collagen synthesis; and third, within the blood vessels in LS-affected areas, there is increased deposition of collagen type V alongside a reduction in ECM1 expression, resulting in a decreased content of elastic fibres [18,28,31,32]. Here, FOXO3 is linked to neoplasm.