SIX2 and neoplasm: Blockage of ITGβ4 also activated components of WNT signaling (CSNK2A1, WNT4, CSNK2B, WNT10A, CSNK1D, and CSNK1G2), which are required for commitment (Figure S7C, Supporting Information).[51] Finally, in mouse recipients of WT SIX2+CITED1+ cells, the speed of tumor growth tended to be enhanced by anti‐ITGβ1 (Figure 3I) versus mice treated with anti‐ITGβ4.