In tumor tissues, some genetic or epigenetic changes in FGFR, such as gene amplification, mutations, fusions, or rearrangements, as well as histone methylation or noncoding RNAs mediate the elevation of FGFR expression, lead to aberrant activation of FGFR, which upregulates a number of unique pathways, such as the PI3K/AKT, Ras/ERK, PLCγ, STAT, and Wnt/β‐catenin signaling pathways, to promote tumorigenesis and progression, including tumor cell proliferation, tumor cell invasion, tumor cell migration, EMT, angiogenesis, metabolic changes, chemoradiotherapy resistance, and tumor cell stemness. This evidence concerns the gene SOAT1 and neoplasm.