CD99 and neoplasm: EWS-FLI1 participates in maintaining the high expression of CD99 not only through transcriptional regulation of CD99 but also through indirect mechanisms, such as the repression of miR-30a-5p, which targets the 3′ untranslated region of CD99 [17], supporting evidence that crosstalk between these two molecules is required for the malignancy of this tumor.