PTPRC and neoplasm: However, decreased proliferation was observed upon the CRISPR-Cas9 knockout of IGF1R in several single-cell clones of both the IGF1R-WT and CD45+ HMCL U-266 and the IGF1R-mutant HMCL L-363, supporting the observation that MM depends on IGF1R and that IGF1R is preferentially essential for MM compared to other neoplasias [42].