Specifically, the N terminus of LSD1 (a.a. 1–170) was found by Waterbury et al., (28) to engage with its adjacent structured domains through a series of transient interactions, thereby establishing a cell-based molecular function for this IDR element to act as a “fuzzy” molecular switch, regulating LSD1-transcription factor (GLF1B, C/EBPa, RUNX1, and PU.1) interactions, modulating silencing-enhancer activity across cis-regulatory landscapes, and impacting AML cancer-associated differentiation. This evidence concerns the gene SPI1 and acute myeloid leukemia.