We speculated that the activation of RTKs contributed to JAK over-expression in patient 1’s tumor.18,19 Increased expression of ATF1 and its transcriptional targets, TOP2A, CALCA, and IL6, was observed, presumably as a result of constitutive transcriptional activation by EWSR1-ATF1 (Fig 3A; Appendix Fig A3). Here, ATF1 is linked to neoplasm.